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Review

Allergic Disorders and Systemic Lupus Erythematosus: Common Pathogenesis and Caveats in Management

by
Hee-Jae Jung
1,*,
Saja Mustafa Ali
2,
Reena Khianey
3 and
Jamal Mikdashi
3
1
Department of Medicine, Midtown Campus, University of Maryland Medical Center, Baltimore, MD 21201, USA
2
Division of Rheumatology & Clinical Immunology, Department of Medicine, University of Maryland Medical Center, Baltimore, MD 21201, USA
3
Division of Rheumatology & Clinical Immunology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
*
Author to whom correspondence should be addressed.
Allergies 2025, 5(2), 10; https://doi.org/10.3390/allergies5020010
Submission received: 9 November 2024 / Revised: 22 January 2025 / Accepted: 21 March 2025 / Published: 1 April 2025
(This article belongs to the Section Diagnosis and Therapeutics)
Browse Figure
Versions Notes

Abstract

:
(1) Background: Allergic disorders and systemic lupus erythematosus (SLE) are immune dysregulation conditions that are increasingly prevalent, with growing evidence suggesting shared pathogenesis. (2) Results: Patients with SLE have a higher risk of allergic conditions, particularly allergic rhinitis and asthma; notably, children born to mothers with SLE show an increased asthma risk. This association appears linked to shared mechanisms involving T-helper 2 cells, IgE, human leukocyte antigen, genetic factors, and environmental triggers. Various medications used in allergic disorders and SLE have benefits in both diseases. Many SLE medications benefit allergic dermatitis. Meanwhile, omalizumab used for severe asthma may reduce SLE activity. (3) Conclusions: More research is essential to clarify the shared pathways and cross-benefits of treatments for allergic disorders and SLE. Novel treatment strategies are warranted to clarify the roles of biologic treatment in allergic disorders in the setting of SLE.

1. Introduction

Allergic disorders have been on the rise since the late 1970s in the US, along with other autoimmune diseases such as multiple sclerosis, Crohn’s disease and type 1 diabetes [1]. A study based on the CDC registry from Olmsted, MN, USA showed that the incidence and prevalence of systemic lupus erythematosus (SLE) have been increasing as well [2]. Both allergic diseases and SLE impose a significant burden on both the patient and society [3,4]. With increasing incidence in both disorders, physicians are more likely to encounter patients with both conditions.
Allergic disorders, such as allergic rhinitis and asthma, are thought to be part of a spectrum of systemic inflammatory disorders with a common pathophysiology [5,6]. In particular, allergic disorders are thought to be a T-helper 2 (Th2) cell-mediated immune response against environmental antigens [7]. SLE is a complex autoimmune disease whose pathogenesis is still under investigation [8,9]. So far, T-cell dysregulation has widely been regarded as one of the causes of SLE [8,10]. As allergic disorders and autoimmune disorders such as SLE are both thought to be disorders of immune regulation, it is important to understand the association between these conditions and their implications [11].
In this review, the authors will summarize the evidence that has been published so far on the relationship between major allergic disorders, such as allergic rhinitis or asthma, and SLE. Drug hypersensitivity reactions are excluded given the scope of the review. Moreover, this review article will focus on the implications of allergen-mediated therapy in patients with autoimmune disorders and the implications of SLE treatment.

2. Associations Between Allergic Disorders and SLE

There have been several studies in the past looking at whether SLE and allergic disorders were associated, given the belief that allergies and autoimmunity share a common immunological pathway. So far, there has been conflicting evidence in the literature. Several studies have shown that allergic disorders such as allergic rhinitis, asthma, allergic conjunctivitis, dermatitis and others are more common in SLE than in patients without SLE [12,13], while some studies have shown that the incidence of allergic disorders in SLE patients is comparable to that in the general population [14,15,16].
The conflict in the literature might arise from small sample sizes, as most of the studies were based of sample sizes of a minimum of 44 to a maximum of 198 [12,13,14,15,16]. In studies based on larger sample sizes or meta-analyses, associations between allergic disorders and SLE show statistical significance. Krishna et al. reported that patients with allergic disorders had higher long-term risks of SLE in a large population-based study [6]. The associations between various allergic disorders and SLE are summarized in Table 1 [17,18,19,20,21,22].
Further evidence of the association between SLE and specific allergic disorders will be discussed in the following segments.

2.1. Allergic Rhinitis (AR) and SLE

There has been a systematic review and meta-analysis that showed a statistically significant association between SLE and AR [19]. The study looked at eight studies (of which one was a cohort study and seven were case–control studies) to evaluate the risk of incident SLE among patients with AR. They concluded that patients with AR had an approximately 1.4-fold increased risk of being diagnosed with SLE. There were limitations to the meta-analysis as the incorporated studies relied on patient self-reports and diagnostic codes in identifying AR [22,23,24]. These results were not replicated in the pediatric population, which may suggest that a different pathophysiology may be present between adults and the pediatric population [25].

2.2. Asthma and SLE

Asthma and SLE have been found to affect both disease states; patients with SLE have a higher tendency to develop asthma and vice versa. Shen et al. reported an increased risk of asthma in patients with SLE in a database-based study using insurance claims and verified SLE patient cohorts [26]. A total of 52,888 SLE patients were followed up with for 11 years. When adjusted for comorbidities, sex and age, patients with SLE had a 2.54 times higher statistically significant risk of developing asthma. When stratified into age groups, younger patients were at a higher risk of developing asthma [26].
A meta-analysis using the Medline and EMBASE databases by Charoenngam et al. showed that patients with asthma had a statistically higher risk of SLE compared to those without asthma, with a pooled odds ratio of 1.37 [20].
Pediatric patients born to mothers with SLE have a higher risk of developing asthma. One study using the Swedish register database looked at 12,000 singleton live births from 2001 to 2013. The study showed that children born to mothers with SLE had a 1.46 times statistically higher risk of being diagnosed with childhood asthma [27]. This highlights a possible common genetic and environmental component in SLE and asthma’s pathogenesis.

3. Immunoglobulin E in Allergic Disorders and SLE

The pathophysiology behind SLE is thought to be driven by various mechanisms, including dysregulated T-cells, autoreactive antibody-producing B-cells, neutrophils and plasmacytoid dendritic cells [10]. It is thought that type 1 interferons are the main drivers of SLE pathogenesis, stimulated by autoantibodies or the production by neutrophils [28,29,30,31]. A comparison of the key immunological components driving allergic disorders and SLE is summarized in Table 2 [32,33,34].
Allergic diseases are mediated by immunoglobulin E (IgE), with the subsequent activation of mast cells and basophils. This leads to the release of inflammatory cytokines and other mediators, causing acute inflammation and clinical features [35]. There have been several studies showing that IgE plays a key role in the development of autoimmune conditions in relation to the activation of type 1 (Th1) and type 2 (Th2) helper T-cells [13,36].
Evidence has been conflicting regarding whether elevated IgE levels represent a common mechanism between allergic disorders and SLE. Wongtrakul et al. proposed that increased IgE production with the subsequent activation of inflammatory pathways is a common mechanism between AR and SLE [19]. Bruber et al. also reported increased anti-IgE antibodies in SLE patients [37]. Meanwhile, Wozniacka et al. showed contradicting evidence as they found no statistically significant increase in IgE levels in SLE patients in remission compared to normal controls [38]. Moreover, Wozniacka et al. also showed that the prevalence of allergic diseases was not higher in patients with SLE than in the general population [38]. A previous small-scale study involving 50 patients with SLE compared to healthy controls also did not show that patients with SLE had an increased rate of allergic disorders [15]. Wonziacka et al. attributed the contradictory findings to geographical and environmental differences and subsequently differences in the types of allergen exposure [38].
It is important to note that Wozniacka et al. showed that SLE patients with active disease had statistically higher serum IgE concentrations compared to inactive patients [38]. This suggests that IgE may have a role in SLE pathogenesis, especially in terms of disease activity. Another small-scale study by Elkayam et al. also supports this, as they found an increase in IgE concentrations in patients with active lupus nephritis compared to patients in remission [14].
More recently, autoreactive IgE has emerged as a pathophysiologic mechanism of SLE by activating basophils and plasmacytoid dendritic cells [39]. Autoreactive IgE has been shown in mouse models to induce lupus-like nephritis, presumed to be due to basophil activation by autoreactive IgE [40]. One study showed that SLE patients had increased numbers of activated basophils in the lymph nodes and spleen, which are involved in T- and B-cell activation [40]. Dema et al. showed that autoreactive IgE against dsDNA, Sm and SSA was associated with clinically active SLE disease [41]. Autoreactive IgE immune complexes are thought to stimulate plasmacytoid dendritic cells by activating Fc epsilon receptors (FcεRI), inducing type I interferon production [42]. Thus, increased autoimmunity via IgE may have a role in the pathogenesis of SLE.

4. Common Risk Factors of Allergic Disorders and SLE

Genetics have been shown to play a role in the shared pathogenesis of allergic disorders and SLE. Some studies have shown that human leukocyte antigen (HLA) genotypes are significant independent risk factors for the development of allergic disorders and SLE [43,44]. Furthermore, other studies have shown that genetic polymorphisms are shared between SLE and allergic disorders. Kreiner et al. discovered a single-nucleotide polymorphism (SNP) in the HLA-B gene to result in an increased risk for the development of both allergic disorders and SLE, at a false discovery rate of less than 0.05 [45]. Chen et al. identified ENTPD1 as a hub gene between AR and SLE in a large database study [46]. Rossides et al. observed that children born from SLE mothers had a higher risk of developing asthma, which may further support the notion of common genetic risk factors for allergic disorders and SLE [27].
However, some genetic polymorphisms that increase the risk for SLE may be protective in developing allergic disorders. A study based on the GWAS data of individuals of European ancestry demonstrated that SNPs associated with SLE had protective effects against AR [47]. This is contradictory to what has been widely known. The authors of the study attribute this to differences in the study design and the confounding effects of aging and gene–environment/gene–gene interactions [47].
There are also environmental factors that are shared between allergic disorders and SLE. One of the most reversible and easily identified ones in the outpatient setting is cigarette smoking. Cigarette smoking alone is a well-described risk factor for asthma and SLE [48,49,50]. Ambient air particles are also reported to represent risk factors for the development of both SLE and allergic rhinitis [51,52]. There may be more environmental factors that are uncovered in the future.
The authors speculate that SLE and allergic disorders may have an overlap (Figure 1).
So far, what studies have shown is that SLE and allergic disorders are related, sharing a common pathogenesis mediated by IgE and Th2 cells. Various authors speculate that patients with certain genetic predispositions, who are exposed to certain environmental triggers, are more susceptible to both SLE and allergic disorders. It is possible that dysfunction of the epithelial barrier may contribute as the linkage between genetic/environmental factors and autoimmunity [53]. Viruses are also emerging as a mediator in developing autoimmunity in allergic disorders and SLE [54,55,56,57]. The effects of environmental factors in SLE development are still unclear, with limited information [58]. As such, further studies are needed to elucidate the common molecular pathways between allergic disorders and SLE.

5. Treatment Options in Allergic Disorders and SLE

5.1. Allergy Therapy and SLE

5.1.1. Allergen Immunotherapy

As allergic disorders and SLE are shown to have a statistical correlation and suspected to share a common pathogenesis, this raises the question of whether the treatment modalities for one disease affect the other disease’s process.
Allergen immunotherapy (AIT) is thought to work by inducing allergen-specific IgA and IgG that compete with allergen-specific IgE [34]. By introducing specific allergens to the patient, they will stimulate TLR-4 and -9 to induce a pro-regulatory phenotype [59,60]. These dendritic cells induce regulatory T-cells that inhibit Th2 cells and secrete IL-10 to induce B-cells to undergo isotype switching [61].
It is generally not recommended to initiate AIT in active autoimmune disease, and providers should be cautious in initiating AIT in patients with autoimmune diseases in remission, as per the European Academy of Allergy and Clinical Immunology (EAACI) guidelines [62]. Thus, there has been scant research into the efficacy of allergen immunotherapy (AIT) in SLE patients. A case series by Fujioka et al. showed that AIT is safe and effective in patients with stable autoimmune conditions [63]. A limitation to this research was that SLE patients were not included. There is evidence that AIT does not induce autoimmune diseases; thus, it could be assumed that it may not cause further flares in SLE patients [64].
Furthermore, there have been speculations regarding the use of the immunological phenomenon behind AIT in SLE management by inducing regulatory T-cell development [65]. Although AIT is generally not recommended in standard practice for SLE patients, it may hold some benefit in SLE management depending on the target allergen. Further research would be needed on an individual allergen-specific basis.

5.1.2. Omalizumab

Omalizumab, which is a humanized IgG1 monoclonal antibody that blocks IgE from binding to FcεRI, is a Food and Drug Administration (FDA)-approved drug for the treatment of severe asthma and chronic idiopathic urticaria [66,67]. A randomized clinical trial by Hansi et al. showed that omalizumab is well tolerated in patients with SLE and might also improve SLE activity [68].

5.1.3. Baricitinib

Baricitinib, which is an oral selective Janus kinase 1 and 2 inhibitor, is approved for the treatment of atopic dermatitis. Recent randomized clinical trials showed that baricitinib can be safely administered in SLE patients with or without active disease [69,70]. Its long-term efficacy in the control of SLE is still uncertain and warrants further studies with higher-quality evidence.

5.2. SLE Treatments and Allergic Disorders

5.2.1. Hydroxychloroquine

Hydroxychloroquine (HCQ) is the recommended medication in all patients with SLE as per the European Alliance of Associations for Rheumatology (EULAR) guidelines [71]. It is presumed that HCQ reduces antigen processing in macrophages and other antigen-processing cells (APCs). This would lead to a reduction in peptide–MHC protein complex formation, which is required for CD4+ T-cell stimulation [72]. More recently, other mechanisms of action have been uncovered and proposed. HCQ may trigger mammalian target of rapamycin complex 1 (mTORC1) and calcium-mediated lysosome biogenesis under stress [73]. HCQ also is known to impair autophagy flux, reducing the amount of autoantigens to be exposed [74].
In the 1980s and 1990s, researchers examined the use of hydroxychloroquine in the treatment of asthma [75,76,77]. A study compared asthma patients receiving standard inhaled corticosteroid therapy with as-needed β2-adrenergic agonists with HCQ or placebo treatment. They showed a statistically significant improvement in the morning peak flow rates, β2-adrenergic agonist use and mean IgE levels. However, the study was limited due to the small sample size of 17. This outcome was not replicated in a double-blind crossover trial by Roberts et al., which was also limited by a small sample size of nine [76]. During the COVID-19 pandemic, HCQ resurfaced as a possible adjuvant therapy for COVID-19, and some researchers noted benefits in asthma control in those who were on HCQ for COVID-19 [78].
Recently, an in vitro study of asthma patients showed increased rates of autophagy in sputum granulocytes, peripheral blood cells and peripheral blood eosinophils. The study also demonstrated that autophagy was suppressed by HCQ [79]. As the release of self-antigens through apoptosis and autophagy is proposed to be one of the driving forces of SLE, there might be a role of increased autoreactive IgE formation as one of the mechanisms behind asthma pathogenesis [10].
HCQ is a relatively cheap medication that is widely used in SLE patients. It may also have a role in asthma patients; however, data on its benefits are very limited. Large-scale studies examining HCQ in asthma may lead to the development of new treatment options. In relation to other atopic diseases, HCQ use has not been well examined in allergic rhinitis or atopic dermatitis.

5.2.2. Methotrexate

Methotrexate (MTX) is a folic acid antagonist that is also widely used in SLE. The EULAR guidelines recommend using MTX as the second line after HCQ for SLE patients [71].
MTX can be used in the treatment of atopic dermatitis in elderly patients as an alternative option to biologics [80]. It has off-label use in atopic dermatitis, and many research groups have suggested a starting dose of 10 mg/week, followed by 15~25 mg/week maintenance doses [81].
MTX use in asthma have been studied as a steroid-sparing therapy in asthma patients dependent on oral corticosteroids. A Cochrane review showed that, although MTX had a statistically significant steroid-sparing effect, the reduction was not large enough to offset the steroid side effects (reduction of around 5 mg of oral steroids per day) [82]. Later, a double-blind, randomized, placebo-controlled study showed a similar steroid-sparing effect, but with a larger reduction in doses (reduction of 9.5 mg/day for oral steroids) [83]. However, society guidelines recommend against the use of MTX in severe asthma due to the higher risk of adverse effects compared to the benefit in steroid reduction [84].
Although MTX has shown some efficacy in atopic dermatitis and asthma, its adverse effects make it unsuitable for widespread use. SLE patients with atopic dermatitis or severe asthma may benefit from MTX as part of their SLE management.

5.2.3. Azathioprine

Azathioprine is a purine analog that acts by disrupting nucleic acid synthesis. It is also used in SLE for immunosuppression, but to a lesser degree [71]. Among allergic disorders, it has been studied most extensively in the setting of atopic dermatitis. Although it has been shown to have some benefit in atopic dermatitis, the overall risks of azathioprine outweigh the benefits of its use in severe refractory atopic dermatitis and it is not recommended for use as per the latest guidelines [32]. However, if azathioprine is used for SLE management, it may also have some beneficial effects in managing refractory atopic dermatitis.
There are limited data on the use of azathioprine in asthma. A Cochrane review of two small randomized clinical trials showed a lack of evidence of the steroid-sparing effects of azathioprine in chronic asthma [85].

5.2.4. Mycophenolate Mofetil

Mycophenolate mofetil (MMF) is a inosine monophosphate dehydrogenase inhibitor that leads to the suppression of de novo guanine nucleotide synthesis. MMF works as an immunosuppressive agent as B-cells and T-cells rely on de novo nucleic acid synthesis. It is also a common medication used in managing SLE patients [71].
MMF has been reported to have some limited benefits in the management of atopic dermatitis. A recent meta-analysis on MMF use in atopic dermatitis showed that it may be effective in managing treatment-resistant atopic dermatitis that needs systemic immunosuppression. The average mean time for a response to treatment was 6.8 weeks, with relapse occurring in 8.2% of the studied cases [86]. As SLE patients are often on MMF for prolonged periods of time, it may have an additional beneficial effect in controlling atopic dermatitis.
Data on MMF for asthma are limited. An animal study using murine models showed that MMF may attenuate airway inflammation and hyperresponsiveness [87]. It is speculated that MMF inhibits CD4+ T-cell-mediated immune responses in the lungs, leading to the suppression of asthma development. The benefits in humans with difficult-to-control asthma need to be further studied.

5.2.5. Anifrolumab

Anifrolumab is a novel human monoclonal IgG that binds to the interferon alpha receptor (IFNAR), which leads to the blockage of type 1 interferon signaling (IFN-1). It has been approved by the Food and Drug Administration for the treatment of SLE in adults and is recommended for use in SLE as per the EULAR guidelines [71,88].
The use of anifrolumab has not been examined well in the setting of allergic disorders. One of the main pathophysiologic mechanisms underlying allergic disorders is Th2 cell-mediated inflammation from allergen-specific IgE. Recent research showed that IFN-1 might have a role in suppressing Th2 cell-mediated immune responses and may be a new treatment option for steroid-resistant asthma [89]. The authors speculate that, as anifrolumab blocks the action of IFN-1, it might adversely affect patients with allergic disorders. The efficacy of anifrolumab was studied in three major trials, TULIP-1, TULIP-2 and MUSE [88,90,91]. Whether anifrolumab caused or worsened allergic disorders was not examined as part the safety profile in these trials. Further studies are needed to determine whether anifrolumab negatively affects those with allergic disorders.

5.2.6. Belimumab

Belimumab is a monoclonal antibody that acts as an antagonist to soluble B-cell activation factor (BAFF). BAFF stimulates the survival and differentiation of B-lymphocytes into immunoglobulin-producing plasma cells [92]. It was approved by the FDA for the treatment of adults with active lupus nephritis and has been widely incorporated into various guidelines for use in SLE [93].
There is a lack of data regarding belimumab in allergic disorders, but it may have a role in allergic asthma management. Recent studies show that BAFF might have a role in asthma development [94]. Although further studies need to be conducted regarding the exact role of BAFF in asthma, some authors speculate that belimumab may play a role in asthma management. The study of asthma in patients on belimumab will help to further elucidate the role of BAFF in asthma pathogenesis.

5.2.7. Rituximab

Rituximab is one of the most widely used treatment modalities in SLE. There have been several case reports of rituximab benefitting asthma control in the setting of other autoimmune diseases, such as eosinophilic granulomatosis with polyangiitis (EGPA) and IgG4-related disease [95,96,97]. Although the evidence in SLE remains promising, rituximab may have some benefit in allergy control in SLE patients. This would need to be further explored in the future. A summary of the aforementioned medications commonly used in SLE and their benefits in allergic disorders is presented in Table 3.

6. Conclusions

The bidirectional relationship between allergic disorders and SLE is complex and needs further research. In the literature, autoreactive IgE has been noted as key in explaining the relationship between the two diseases. The pathophysiology of SLE is rooted in the autoantibody production of self-antigens, and allergic disorders are defined by IgE-Th2 mediated inflammation. The study of allergic disorders regarding Th2-mediated inflammation may identify further immune response pathways to be studied in SLE. It is also not well known whether the relationship between allergic disorders and SLE has a component of causality. Future research on whether autoreactive IgE is responsible for immune dysfunction or simply a byproduct of dysregulated adaptive immunity might help to further elucidate this relationship.
Some common medications used in SLE have been found in other allergic disorders to have a benefit. Most of these medications carry a high risk of adverse effects that does not justify their use in patients with only allergic disorders. They may offer a ‘two-birds-with-one-stone’ management option for SLE patients with severe allergic disorders. Further studies are needed to examine their long-term effects in SLE patients with allergic disorders.
AIT can be a double-edged sword. It is a treatment option that induces an immune response, which could mask the effects of IgE with other immunoglobulin subtypes or induce regulatory immune cells. As SLE is thought to arise from autoantibody formation against autoantigens, it is also possible that AIT might be used to induce anergy against such autoantigens. The mechanism behind AIT and the way in which it induces regulatory immune cells need to be further studied, along with further clarification of the main driving pathogenic autoantigens in SLE.

Author Contributions

Conceptualization, J.M. and H.-J.J.; writing—original draft preparation, H.-J.J.; writing—review and editing, S.M.A., R.K. and J.M.; visualization, H.-J.J.; supervision, R.K. and J.M.; project administration, H.-J.J. and J.M. 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.

Conflicts of Interest

The authors declare no conflicts of interest.

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Allergies 05 00010 g001
Figure 1. Schematic of overlapping pathologies in SLE and allergic disorders.
Figure 1. Schematic of overlapping pathologies in SLE and allergic disorders.
Allergies 05 00010 g001
Table 1. Allergic disorders commonly observed with SLE.
Table 1. Allergic disorders commonly observed with SLE.
Allergic DisorderIncident Risk
Allergic rhinitis1.4
Asthma1.37~2.54
Allergic conjunctivitis1.43
Atopic dermatitis1.46~2.13
Table 2. Key immune cells in allergic disorders and SLE.
Table 2. Key immune cells in allergic disorders and SLE.
Immune CellsAllergic DisordersSLE
B-cells IgE productionAutoantibody production
Long-lived plasma cells
Th1 cells-Promotion of oxidative stress
Interferon-γ (IFNγ) production
Th2 cellsStimulate B-cells via IL-4, IL-13 to stimulate B-cell class switching to IgE
Eosinophil recruitment		Decrease in IL-4-producing cells
Th17 cells-Increased IL-17 production
Regulatory T-cells-Unclear
T-follicular cells-Involved in autoreactive B-cells
CD8+ T-cells-Impaired cytolytic function
γδ-T-cells-High levels in SLE
Neutrophils-Reduced phagocytosis
Reduced removal of apoptotic cells
Type 1 interferon (IFN-1) production
Dendritic cellsAllergen detection and stimulation of Th2 cellsPlasmacytoid dendritic cells produce high levels of IFN-1
Mast cellsActivated by IgE
Release of cytokines, prostaglandins,
leukotrienes and histamines		-
Table 3. Commonly used SLE medications and benefits in major allergic disorders.
Table 3. Commonly used SLE medications and benefits in major allergic disorders.
Medication Used in SLEAllergic RhinitisAsthmaAtopic Dermatitis
HydroxychloroquineNot studied *Possible benefitNot studied
MethotrexateNot studiedSteroid-sparing,
high risk profile		Off-label use
AzathioprineNot studiedNo steroid-sparing effectMay have benefit
High risk profile
Mycophenolate mofetilNot studiedPossible benefitSteroid-sparing,
high risk profile
AnifrolumabNot studiedTheoretical harmNot studied
BelimumabNot studiedTheoretical benefitNot studied
RituximabNot studiedPossible benefitNot studied
* Not studied: to our knowledge, there is a lack of or absence of evidence for use in the respective allergic disorders.
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Jung, H.-J.; Mustafa Ali, S.; Khianey, R.; Mikdashi, J. Allergic Disorders and Systemic Lupus Erythematosus: Common Pathogenesis and Caveats in Management. Allergies 2025, 5, 10. https://doi.org/10.3390/allergies5020010

AMA Style

Jung H-J, Mustafa Ali S, Khianey R, Mikdashi J. Allergic Disorders and Systemic Lupus Erythematosus: Common Pathogenesis and Caveats in Management. Allergies. 2025; 5(2):10. https://doi.org/10.3390/allergies5020010

Chicago/Turabian Style

Jung, Hee-Jae, Saja Mustafa Ali, Reena Khianey, and Jamal Mikdashi. 2025. "Allergic Disorders and Systemic Lupus Erythematosus: Common Pathogenesis and Caveats in Management" Allergies 5, no. 2: 10. https://doi.org/10.3390/allergies5020010

APA Style

Jung, H.-J., Mustafa Ali, S., Khianey, R., & Mikdashi, J. (2025). Allergic Disorders and Systemic Lupus Erythematosus: Common Pathogenesis and Caveats in Management. Allergies, 5(2), 10. https://doi.org/10.3390/allergies5020010

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