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Review

Complement at the Nano–Neuroimmune Interface: A Hypothesis-Driven Perspective on Opioid Use Disorder

by
Alexander Jacob
,
Harbir Singh
,
Poolakkad S. Satheeshkumar
,
Aum Champaneri
,
Rahul K. Das
,
Ravi K. Aalinkeel
,
Supriya D. Mahajan
and
Jessy J. Alexander
*
Department of Medicine, Jacobs School of Medicine & Biomedical Sciences, SUNY University at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USA
*
Author to whom correspondence should be addressed.
Immuno 2026, 6(1), 14; https://doi.org/10.3390/immuno6010014
Submission received: 26 December 2025 / Revised: 9 February 2026 / Accepted: 10 February 2026 / Published: 13 February 2026
(This article belongs to the Section Innate Immunity and Inflammation)
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Abstract

The complement system is a central component of innate immunity with established roles in host defense and emerging functions in neurodevelopment, synaptic remodeling, and neuroimmune communication within the central nervous system (CNS). In parallel, advances in nanotechnology have not only enabled targeted strategies for CNS drug delivery but have also revealed that many nanomaterials interact with and activate complement, influencing biodistribution, safety, and inflammatory responses. Opioid use disorder (OUD) is increasingly recognized as a condition associated with chronic neuroimmune dysregulation involving glial activation, altered cytokine signaling, and blood–brain barrier (BBB) disruption. However, direct experimental or clinical measurements of complement activation in OUD remain limited. Current evidence linking complement pathways to opioid exposure is derived largely from indirect observations, including transcriptomic alterations, glial phenotypes, and inflammatory signatures in preclinical and translational models, which collectively suggest, but do not yet definitively establish, complement involvement in opioid-induced neuroimmune signaling. This review synthesizes current knowledge at the intersection of complement biology, nanomedicine, and opioid-associated neuroimmune changes. It distinguishes well-established mechanisms of complement activation by nanomaterials from emerging and inferential evidence linking complement signaling to opioid exposure. This hypothesis-generating framework integrates complement signaling with opioid receptor and TLR4 pathways in glial and endothelial compartments, examining their potential protective and pathological CNS roles while outlining the translational promise and current evidence gaps of complement-aware nanotechnologies for addiction neuroscience.

1. Introduction

The complement system is a conserved innate immune network [1,2] that detects pathogens, altered self-surfaces, and immune complexes, triggering opsonization, inflammation, and lytic activity [3,4,5]. Beyond host defense, complement is increasingly recognized as an active regulator of CNS homeostasis, synaptic remodeling, and glial-neuronal communication, with dysregulation implicated across neuroinflammatory and neuropsychiatric conditions [6,7,8,9,10,11].
Nanotechnology has emerged as a transformative platform for drug delivery, vaccine development, and molecular imaging [12]. A substantial body of preclinical and clinical evidence demonstrates that many nanomaterials, including liposomes, polymeric nanoparticles, lipid nanoparticles, dendrimers, inorganic nanostructures, and hybrid materials can activate complement through classical, lectin, or alternative pathways, thereby influencing nanoparticle biodistribution, safety, and inflammatory outcomes [13], leading to complement activation-related pseudoallergy (CARPA) [14], altered pharmacokinetics, and inflammatory reactions that can be consequential for CNS delivery, where immune activation at the BBB or within neural tissue can have disproportionate consequences.
Opioid use disorder (OUD) [15] is associated with chronic neuroimmune dysregulation, including sustained glial activation, altered cytokine signaling, and blood–brain barrier (BBB) dysfunction [16,17,18,19,20,21]. While direct measurements of complement activation in OUD remain limited, converging transcriptomic, cellular, and inflammatory data from opioid exposure models suggest potential intersections between opioid signaling, complement pathways, and neuroimmune circuits.
Accordingly, this review distinguishes the well-established interactions between nanomaterials and complement activation from the more emergent and inferential links between complement pathways and opioid-associated neuroimmune alterations, using this integrated perspective to identify mechanistic convergence points, translational opportunities, and priority knowledge gaps at the proposed nano–neuroimmune interface.

2. Complement Biology in Systemic and CNS Immunity

The complement system plays a significant role in peripheral and central nervous system immunity function. The role of the complement system has been related to both neuroprotective and neuroinflammatory functions [22,23]. There has also been correlative studies into the relation between the complement system and the onset of various of neurological and psychiatric disorders.

2.1. Overview of Complement Activation Pathways and Regulators

The complement system can be activated through three principal pathways, the classical, lectin, and alternative pathways, which differ in their mode of initiation and converge at C3 cleavage (Figure 1). All three pathways continue in an identical fashion with the generation of the membrane attack complex and other downstream effector functions. Regulatory proteins are located at strategic points to prevent excessive complement activation. Detailed molecular descriptions of these pathways have been extensively reviewed elsewhere and are not reiterated here [1,24,25,26,27,28]. Several features of complement activation are particularly relevant from the perspective of nanomaterial interactions. First, complement can be triggered in an antibody-independent manner through direct adsorption of complement proteins onto nanoparticle surfaces, frequently engaging the alternative and lectin pathways. Second, surface chemistry, curvature, charge, and protein corona composition strongly influence C3 deposition and pathway bias. Third, complement amplification and inadequate regulation on artificial surfaces can result in disproportionate inflammatory signaling despite minimal initial activation. In the context of opioid use disorder, these surface and context-dependent features of complement activation are particularly relevant, as chronic opioid exposure is associated with sustained neuroimmune activation and inflammatory amplification mechanisms that may intersect with complement signaling despite the current scarcity of direct evidence.

2.2. Complement in the CNS

Complement activity within the CNS is now recognized as a locally regulated process, supported by the endogenous synthesis of complement components and receptors by neurons, glial cells, and vascular endothelium [29,30,31,32]. Rather than functioning solely as an effector of immune defense, CNS complement signaling operates as a modulatory system that influences synaptic remodeling, cellular crosstalk, and neuroinflammatory tone, including endothelial permeability and leukocyte recruitment [33,34]. In contrast to the periphery, complement activity in the CNS is shaped by spatial confinement, cell-type specific expression patterns, and a distinct balance of regulatory proteins, rendering complement signaling highly context dependent. These features allow complement to exert both homeostatic and pathological effects depending on the timing, magnitude, and cellular localization of activation. This conceptual framework, viewing complement as a context sensitive neuroimmune modulator rather than a uniform effector, provides the basis for understanding how complement activation may influence CNS responses to nanomaterials and intersect with opioid-associated neuroimmune alterations. Specific mechanistic examples and disease-relevant applications are discussed in subsequent sections [35,36,37,38].

3. Complement Activation by Nanomaterials

Nanomaterials engage the complement system (Figure 2) through surface-driven mechanisms that depend on physicochemical properties, protein corona composition, and biological context. While numerous studies have documented complement activation by diverse nanoparticle classes, the pathways engaged and downstream consequences differ substantially across material types, with important implications for CNS delivery [13].

3.1. Liposomes, Lipid Nanoparticles and Complement

Liposomes and lipid nanoparticles frequently activate complement through antibody-dependent classical pathway engagement or lectin pathway recognition of surface-exposed lipids and glycans, contributing to infusion reactions and accelerated blood clearance [39,40]. Polymeric nanoparticles often favor alternative pathway amplification driven by C3 adsorption and insufficient regulatory control, whereas inorganic nanomaterials [41] (e.g., iron oxide, silica, gold) can trigger mixed or noncanonical activation patterns depending on surface curvature and charge density. Upon exposure to biological fluids, plasma proteins including complement proteins, immunoglobulins, pentraxins (e.g., CRP), and glycoproteins adsorb onto nanoparticle surfaces, forming a protein corona that dictates subsequent immune interactions [42]. Particle properties such as curvature [43], hydrophobicity, surface charge [44], and pattern density influence the type and conformation of adsorbed proteins, shaping complement recognition. The corona composition determines which complement pathway, classical, lectin, or alternative pathway is preferentially activated [45]. Importantly, these mechanistic differences translate into distinct immunological consequences. Complement activation may promote opsonization and rapid hepatic or splenic clearance, induce systemic inflammatory responses, or modulate endothelial and glial signaling relevant to CNS exposure. In the context of CNS drug delivery, excessive complement activation may limit brain bioavailability, whereas controlled or subthreshold activation may influence blood–brain barrier interactions and neuroimmune tone [46]. To highlight these distinctions, Table 1 provides a comparative, non-exhaustive synthesis of representative nanomaterial classes, summarizing dominant complement activation mechanisms and associated immunological consequences, and is intended to illustrate key patterns rather than serve as a exhaustive catalog of the field. This comparative framework emphasizes that complement activation is not a uniform liability of nanomedicine but a tunable interface that can either hinder or shape CNS-targeted delivery strategies.

3.2. Complement Pathway Activation Mechanisms

Nanoparticles activate the classical pathway via mechanisms that include the following: (a) natural IgM or IgG binding to exposed phospholipid head groups or hydrophobic domains [48]; (b) CRP binding, which in turn recruits C1q; and direct C1q surface interactions [49], known to occur for certain polymeric or inorganic nanomaterials. Classical pathway activation generates C4b2a convertase, leading to robust C3 cleavage and downstream inflammation. MBL and ficolins bind to glycan structures on nanoparticle surfaces, and glycoproteins within the protein corona [40]. Activated MASPs then initiate C4 and C2 cleavage. Some carbohydrate-decorated nanoparticles demonstrate preferential lectin pathway engagement.
The alternative pathway is especially relevant for nanomaterials because the spontaneously generated C3b can covalently attach to nucleophilic groups on nanoparticle surfaces, Factor B binding and factor D cleavage form the alternative C3 convertase (C3bBb), and properdin may stabilize this convertase, amplifying activity even on “stealth” surfaces. Many nanomaterials exhibit substantial alternative pathway amplification, making this pathway a key target for nanoparticle engineering.

4. Engineering Nanoparticles to Control Complement Activation

A range of engineering strategies have been developed to modulate complement activation by nanomaterials. These approaches differ substantially in their experimental maturity, mechanistic validation, and translational readiness. For clarity, they are discussed below according to the strength of supporting evidence and degree of clinical or preclinical validation.

4.1. Surface Shielding Approaches

In PEGylation and polymer engineering, dense, brush-like polyethylene glycol (PEG) layers reduce protein adsorption and sterically hinder complement components. However, suboptimal PEG density or conformation can still allow C3b deposition. In addition, PEG architecture (chain length, grafting density, linear vs. branched) influences the shift between classical and lectin pathway activation. Optimizing PEG parameters remains central to minimizing complement activation [50]. On the other hand, Zwitterionic materials (phosphory-lcholine, sulfobetaine) mimic membrane headgroups and exhibit low-fouling behavior [51]. Biomembrane-derived coatings (e.g., erythrocyte or platelet membranes) also reduce C1q and MBL recognition and can suppress alternative pathway activation. However, incomplete suppression of complement activation and delayed immune recognition have been reported, underscoring inherent limitations of passive shielding strategies.

4.2. Display of Complement Regulatory Proteins

More recent approaches include dynamic or stimuli-responsive surface modifications, selective recruitment of regulatory proteins, and context-dependent activation control designed to balance immune evasion with functional bioactivity. Decorating nanoparticles with complement regulators such as CD46, CD55, or CD59 can help reduce/prevent complement activation by accelerating convertase decay, reducing C3b amplification, and blocking MAC assembly [40,48]. These strategies create a local complement-suppressive microenvironment without systemic immunosuppression. However, practical implementation remains constrained by the biochemical instability of surface-bound regulatory proteins during storage and circulation, potential immunogenicity or anti-protein antibody formation, manufacturing and orientation-control challenges, and currently uncertain translational scalability and regulatory feasibility for clinical CNS applications. While conceptually attractive, these strategies are supported primarily by early-stage experimental data and require further validation to establish robustness, safety, and relevance for CNS delivery.

4.3. Control of Physicochemical Properties

Rational control of nanoparticle size, curvature, and surface charge has emerged as a reproducible means of biasing complement engagement, particularly alternative pathway amplification. Particle features strongly influence complement activation. Nanoparticles ~40–250 nm often show stronger complement activation than very small or large particles [48]. Cationic surfaces are more complement-activating than neutral or slightly anionic ones [44]. Highly curved surfaces may expose reactive groups that promote C3b attachment [52]. Rational design of these parameters reduces complement turnover on nanoparticle surfaces, however systematic evaluation across material classes and biological contexts remains limited.

4.4. Temporal or Compartmental Complement Inhibition

Complement inhibitors (e.g., C3 inhibitors [53], C5 blockers [54], C5aR1 antagonists [55]) can be co-administered to reduce acute complement activation during nanoparticle infusion [56]. Emerging strategies include: local release of inhibitors from nanoparticles [57], nanobody-based inhibitors targeted to specific tissues [58], and transient suppression of complement at the BBB or inflamed CNS regions will allow targeted complement inhibition.
Collectively, these engineering strategies highlight complement activation as a tunable interface. Their relevance to CNS drug delivery and to neuroimmune conditions such as OUD depends not only on suppression of systemic complement activation but also on preserving context-dependent immune signaling at the blood–brain barrier and within the CNS.

5. Complement Signaling in Opioid Use Disorder

Current evidence linking complement signaling to OUD varies substantially in methodological strength and derives from human observations, controlled animal studies, and indirect or inferential analyses. To avoid overestimation of association strength, these data are discussed below according to level of evidence.

5.1. Human Observational Evidence

Direct measurements of complement activation in individuals with OUD are scarce. Available human data largely consist of transcriptomic, proteomic, or inflammatory signatures obtained from peripheral tissues or postmortem brain samples, in which complement-related genes or pathways are differentially expressed [59,60]. These findings suggest altered complement-associated signaling in OUD but do not establish causality, temporal dynamics, or functional consequences within the CNS.

5.2. Animal and Experimental Models

Preclinical studies of opioid exposure provide controlled experimental systems in which neuroimmune activation, including glial reactivity [61] and inflammatory signaling pathways that intersect with complement-related mechanisms [62], can be examined. However, the available evidence largely consists of changes in complement component expression or receptor associated signaling following opioid administration, which suggest potential involvement of complement pathways but do not establish causal roles or functional relevance for OUD-related CNS outcomes. In addition, many models rely on acute or high-dose paradigms that may not fully recapitulate the temporal complexity of chronic human OUD. Moreover, direct functional manipulation of complement pathways within opioid models remains limited, further constraining causal interpretation.

5.3. Indirect and Inferential Evidence

Additional support for complement involvement in OUD arises from convergence with broader neuroimmune frameworks, including Toll-like receptor 4 signaling, microglial activation states [16], and synaptic remodeling processes known to engage complement pathways in other neurological contexts [63]. While these parallels provide a mechanistic rationale, they remain inferential and should be interpreted as hypothesis-generating rather than definitive evidence.
Collectively, these data support the possibility that complement signaling participates in opioid-associated neuroimmune dysregulation, while underscoring substantial methodological gaps. Direct, longitudinal, and mechanistic studies are needed to define whether complement activation represents a driver, modifier, or consequence of OUD-related CNS pathology.

6. Intersection of Opioids, Complement, and Neuroimmune Circuits

Opioid exposure has been associated with glial activation and neuroimmune signaling changes that may intersect with complement pathways. Rather than establishing direct causality, current data support a model in which opioids, glial responses, and complement signaling participate in overlapping and potentially reinforcing neuroimmune processes [62,64].

6.1. Glia

Astrocytes respond to complement [65] with increased GFAP expression, modulation of cytokines and chemokines, and altered neurotransmitter regulation (e.g., glutamate uptake). Opioids also modify astrocyte [66] calcium dynamics and receptor expression, raising the possibility of convergent pathways that affect synaptic homeostasis. Even though experimental studies suggest that opioid-induced glial activation can coincide with changes in complement-related gene expression or signaling [67,68], these observations are primarily correlative and whether complement activation is a primary driver, secondary amplifier, or downstream consequence of glial reactivity remains unresolved.

6.2. Synapses

Synaptic plasticity within mesolimbic and corticostriatal circuits is a defining feature of addiction. By analogy to other neuroinflammatory contexts in which complement signaling regulates synapse refinement and elimination [69], complement-dependent mechanisms such as expression of complement receptors (CR3, C3aR, C5aR1) by microglia [70], may, in principle contribute to synaptic remodeling [33,71] or altered circuit function during chronic opioid exposure. However, direct experimental evidence supporting such mechanisms specifically in OUD models remains limited, and extrapolation from other disease contexts should therefore be interpreted cautiously. Such effects, if present, would be expected to alter learning processes underlying reward salience, habit formation, and relapse vulnerability. At present, such links should be viewed as mechanistic hypotheses rather than established pathways in OUD.
Collectively, these observations support a working conceptual framework in which opioids, glial cells, and complement signaling form an interconnected neuroimmune network. Defining the directionality, temporal sequence, and functional relevance of these interactions will require targeted experimental approaches that directly interrogate complement activity in opioid exposure models.

7. Blood–Brain Barrier Mechanisms

Glial cells along with endothelial cells and pericytes form the blood–brain barrier (BBB), which serves as a dynamic interface that regulates molecular and cellular exchange between peripheral circulation and the CNS. In neuroinflammatory conditions, including those with complement dysfunction [72], chronic opioid exposure [21], BBB function may be altered through changes in endothelial signaling, tight junction integrity, and immune–vascular interactions.

7.1. Complement and Opioid Effects on the BBB

Complement activation has been implicated in endothelial activation and vascular inflammation in multiple contexts [73]; however, direct evidence defining how complement signaling modifies BBB integrity in opioid use disorder remains limited. Available data suggest that complement fragments may influence endothelial responsiveness and immune cell trafficking rather than uniformly inducing barrier breakdown.

7.2. Implications for Nanomedicine

Importantly, the BBB should not be viewed solely as a passive barrier or site of pathology. Instead, it represents a context-sensitive regulatory interface where complement activity, neuroimmune signaling, and nanomaterial interactions converge. From a therapeutic perspective, this dual role positions the BBB both as a constraint on CNS drug delivery and as a potential target for modulating neuroimmune tone.
In the setting of nanomedicine, complement activation at or near the BBB may either hinder CNS access through immune clearance or be strategically leveraged to influence endothelial signaling and transport mechanisms. Clarifying these opposing effects will be critical for designing complement-aware delivery strategies aimed at neuroimmune disorders, including opioid use disorder.

8. Complement-Targeted and Nanotechnology-Enabled Therapeutics

Therapeutic strategies at the intersection of complement modulation and nanotechnology span a broad spectrum of developmental maturity, ranging from conceptual hypotheses to clinically validated platforms. To avoid the overinterpretation of readiness, these approaches are discussed below according to level of experimental and translational development.

8.1. Clinically Established and Late-Stage Approaches

Systemic complement inhibitors [53], including C5-targeted biologics and small-molecule regulators [74], are clinically approved for inflammatory and hematologic conditions. While not developed for opioid use disorder, these agents provide proof that complement can be safely and effectively modulated in humans. Their relevance to OUD remains indirect and hypothetical, particularly given limited CNS penetration and the absence of addiction-focused clinical data.

8.2. Preclinical Proof of Concept Strategies

Nanotechnology-enabled delivery systems [13] designed to attenuate complement activation or bias immune responses have demonstrated efficacy in preclinical models of neuroinflammation and CNS drug delivery. These include surface-engineered nanoparticles, biomimetic carriers, and complement-aware formulations that improve pharmacokinetics or modulate endothelial and glial signaling. While encouraging, these studies largely remain at the proof-of-concept stage and have not been systematically evaluated in opioid exposure models.

8.3. Exploratory and Hypothesis-Driven Approaches

Emerging concepts include the targeted delivery of complement modulators to CNS interfaces, circuit-specific nanocarriers, and strategies aimed at fine-tuning rather than suppressing complement activity to preserve physiological neuroimmune functions. At present, these approaches are supported primarily by conceptual models and early experimental data and should be viewed as hypothesis-generating rather than therapeutic candidates.
Taken together, these strategies highlight a translational continuum rather than a near-term therapeutic pipeline. Defining the role of complement modulation in opioid use disorder will require coordinated efforts linking mechanistic validation, circuit-level analysis, and careful assessment of therapeutic risk-benefit profiles.

9. Future Directions

Key priorities include longitudinal human studies measuring complement proteins and function across OUD stages, the development of human-derived organoid models to study complement/opioid/nanoparticle interactions, the systematic characterization of protein coronas under conditions relevant to OUD, the evaluation of complement inhibitors and nanobody-based therapies in OUD-relevant preclinical models, and the improved standardization of nanoparticle complement assays for regulatory and translational work.

10. Conclusions

This review integrates current knowledge at the intersection of complement biology, nanotechnology, and opioid-associated neuroimmune alterations, while emphasizing that direct experimental evidence linking complement modulation to opioid use disorder remains limited. Rather than establishing definitive mechanisms, the available literature supports a conceptual framework in which complement signaling may act as a context-dependent modulator of neuroimmune and synaptic processes relevant to addiction.
Advancing this field will require focused efforts addressing several interconnected priorities: (i) longitudinal cell-type and circuit specific resolved measurements of complement activation in human OUD and in chronic opioid exposure models; (ii) mechanistic studies determining whether complement signaling functions as a driver, amplifier, or downstream consequence of opioid induced neuroimmune changes; (iii) investigation of complement influence on synaptic plasticity within reward-related circuits; and (iv) rigorous evaluation of how nanomaterial design shapes complement activation at the blood–brain barrier and within the CNS. From a translational perspective, rigorous evaluation of how nanomaterial design influences complement activation at the blood–brain barrier and within the CNS will be essential. Future efforts should focus on complement-aware nanomedicine strategies that balance immune modulation with preservation of physiological neuroimmune functions.
Collectively, addressing these gaps will require interdisciplinary approaches integrating immunology, neuroscience, materials science, and addiction biology. Such efforts will be critical for determining whether complement pathways represent viable therapeutic targets or biomarkers in OUD, and for guiding the rational design of next-generation CNS delivery platforms.

Author Contributions

Conceptualization—J.J.A. and S.D.M.; Original draft preparation—S.D.M., R.K.D. and R.K.A.; Writing—H.S., A.J., P.S.S. and J.J.A.; Figure—H.S., A.C. and J.J.A.; Review and editing—J.J.A., A.C., S.D.M. and A.J. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Schematic diagram of the complement system.
Figure 1. Schematic diagram of the complement system.
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Figure 2. Nanoparticle (NP) activates complement pathways. The NP activates all three complement pathways as shown. Mannose binding lectins (MBL) activates the Lectin pathway, Immune complexes (IgG) activate the classical pathway (C1), Alternative pathway is spontaneously activated (C3→C3b).
Figure 2. Nanoparticle (NP) activates complement pathways. The NP activates all three complement pathways as shown. Mannose binding lectins (MBL) activates the Lectin pathway, Immune complexes (IgG) activate the classical pathway (C1), Alternative pathway is spontaneously activated (C3→C3b).
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Table 1. Comparative complement activation by major nanomaterial classes.
Table 1. Comparative complement activation by major nanomaterial classes.
Nanomaterial ClassPredominant Complement Activation MechanismPrimary Immunological Consequence
Liposomes/lipid nanoparticlesClassical and lectin pathway engagement via surface lipids, glycans, or bound IgM/IgGOpsonization, complement activation related pseudoallergy (CARPA [47]), accelerated blood clearance
Polymeric nanoparticlesAlternative pathway amplification driven by C3 adsorption and limited surface regulationSustained complement activation and macrophage uptake
Inorganic nanoparticles (e.g., gold, iron oxide, silica)Mixed or noncanonical activation influenced by surface charge, curvature, and crystallinityInflammatory signaling and deposition of complement activation fragments
DendrimersSurface charge-dependent activation, frequently involving the alternative pathwayDose-dependent inflammatory activation or immune quiescence
Hybrid or functionalized nanomaterialsModulated activation through stealth coatings (e.g., PEGylation, zwitterionic surfaces)Reduced or delayed complement engagement
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Jacob, A.; Singh, H.; Satheeshkumar, P.S.; Champaneri, A.; Das, R.K.; Aalinkeel, R.K.; Mahajan, S.D.; Alexander, J.J. Complement at the Nano–Neuroimmune Interface: A Hypothesis-Driven Perspective on Opioid Use Disorder. Immuno 2026, 6, 14. https://doi.org/10.3390/immuno6010014

AMA Style

Jacob A, Singh H, Satheeshkumar PS, Champaneri A, Das RK, Aalinkeel RK, Mahajan SD, Alexander JJ. Complement at the Nano–Neuroimmune Interface: A Hypothesis-Driven Perspective on Opioid Use Disorder. Immuno. 2026; 6(1):14. https://doi.org/10.3390/immuno6010014

Chicago/Turabian Style

Jacob, Alexander, Harbir Singh, Poolakkad S. Satheeshkumar, Aum Champaneri, Rahul K. Das, Ravi K. Aalinkeel, Supriya D. Mahajan, and Jessy J. Alexander. 2026. "Complement at the Nano–Neuroimmune Interface: A Hypothesis-Driven Perspective on Opioid Use Disorder" Immuno 6, no. 1: 14. https://doi.org/10.3390/immuno6010014

APA Style

Jacob, A., Singh, H., Satheeshkumar, P. S., Champaneri, A., Das, R. K., Aalinkeel, R. K., Mahajan, S. D., & Alexander, J. J. (2026). Complement at the Nano–Neuroimmune Interface: A Hypothesis-Driven Perspective on Opioid Use Disorder. Immuno, 6(1), 14. https://doi.org/10.3390/immuno6010014

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