The Role of Cytokines in Cutaneous T Cell Lymphoma: A Focus on the State of the Art and Possible Therapeutic Targets
Abstract
:1. Introduction
2. IL-1
IL-1 in MF/SS
3. IL-2
IL-2 in MF/SS
4. IL-3
IL-3 in MF/SS
5. IL-4
IL-4 in MF/SS
6. IL-5
IL-5 in MF/SS
7. IL-6
IL-6 in MF/SS
8. IL-7
IL-7 in MF/SS
9. IL-8
10. IL-9
IL-9 in MF/SS
11. IL-10
IL-10 in MF/SS
12. IL-11
IL-11 in MF/SS
13. IL-12
Il-12 in MF/SS
14. IL-13
IL-13 in MF/SS
15. IL-14
IL-14 and MF/SS
16. IL-15 and IL-17
IL-15 and IL-17 in MF/SS
17. IL-16
IL-16 and MF/SS
18. IL-18
IL-18 in MF/SS
19. IL-19, IL-20, IL-22, IL-24, and IL-26
IL-19, IL-20, IL-22, IL-24, and IL-26 in MF/SS
20. IL-21
IL-21 in MF/SS
21. IL-22
22. IL-23
IL-23 in MF/SS
23. IL-24
24. IL-25
IL-25 in MF/SS
25. IL-26
26. IL-27
IL-27 in MF/SS
27. IL-28 and IL-29
28. IL-30
IL-30 in MF/SS
29. IL-31 and IL-8
IL-31 and IL-8 in MF/SS
30. IL-32
IL-32 in MF/SS
31. IL-33
IL-33 in MF/SS
32. TNF-α
TNF-α in MF/SS
33. EGF
EGF in MF/SS
34. FGF
FGF in MF/SS
35. PDGR
PDGRα in MF/SS
36. Interferon Type I, Type II, and Type III
Interferon Type I, Type II, and Type III in MF/SS
37. Discussion
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
Abbreviations
APC | Antigen-Presenting Cell |
CD | Cluster of Differentiation |
CCL | C-C Motif Chemokine Ligand |
CCR | C-C Motif Chemokine Receptor |
CTCL | Cutaneous Cutaneous T cell lymphoma |
CXCL | C-X-C Motif Chemokine Ligand |
EGF | Epdermal Growth Gactors |
FGF | Fibroblast Growth Factors |
JAK | JAnus Kinase |
GAB | GRB2-associated-binding protein |
HDAC | Histone Deacetylases |
HMGB | High Mobility Group Box protein |
ICAM-1 | Intercellular Adhesion Molecule 1 |
IFN | Interferon |
IL | InterLeukin |
IP | Interferon-Inducible Protein |
IT | ImmunoToxin |
LDH | Lactate DeHydrogenase |
MAPK | Mitogen-Activated Protein Kinase |
MDA7 | Melanoma Differentiation-Associated protein 7 |
MF | Mycosis fungoides |
nbUVB | narrow band Ultra Violet type B |
NOS | Nitrogen Oxygen Species |
PBMC | Peripheral Blood Mononuclear Cell |
PI3Ks | Phosphoinositide 3-kinase inhibitors |
PDGF | Platelet-Derived Growth Factors |
PUVA | Psoralen and Ultra Violet type A |
ROS | Reactive Oxygen Species |
SATB1 | Special AT-rich sequence-Binding protein-1 |
STAT | Signal Transducer and Activator of Transcription |
SS | Sézary syndrome |
TAM | Tumor-Associated Macrophage |
TCGF | T cell growth factor |
Tfh | T follicular helper cell |
TGF | Transforming Growth Factor |
TNF | Tumor Necrosis Factor |
Th | (Lymphocyte) T helper (Cell) |
T-Regs | (lymphocyte) T-regulatory cells |
NK | Natural Killer (cell) |
γc | Common gamma chain |
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Cytokine | Function | Role in MF/SS | Potential Targeted Therapies Evaluated |
---|---|---|---|
IL-1 | Pro-inflammatory [17]. | Elevated in treated patient; potential biomarker of photopheresis response [19,20]. | No studies available |
IL-2 | Pro-inflammatory. Upregulate T cells and to increase the cytotoxicity of monocytes and natural killer (NK) [21]. | May have an CTCL suppressive action, but still controversial [22,23]. | AS101 inihbits IL2R and increases IL-2, suggesting an immunosuppressive role [24]. Denileukin Diftitox, which seems to reach a response of 36–40% of CTCLs in some studies [25]. CCR4-IL2 IT, in pre-clinical models seems to be promising in inducing CTCLs remission [26]. |
IL-3 | Pluripotent and hematopoietic factor required for survival and proliferation of hematopoietic progenitor cells [27]. | Unknown. | No studies available. |
IL-4 | Negatively modulates Th1 T cells; skews to a Th2 phenotype of naïve T cells [28]. | Contributes to immune evasion and tumor progression microenvironments (still debated) [29]. Can (with IL-33) induce IL-31 secretions, involved in itch pathogenesis [28,30]. | Anti PD-1 (Nivolumab) could reduce malignant Th2 cells, but it is controversial [31,32]. JAK inhibitor (Ritlecitinib) showed promising effect in reducing Th2 neoplastic cells (IIA trial ongoing) [33]. Dupilumab, by blocking IL-4 and Il-13, could induce an immune system against the tumor and blocking of Th2 cells’ proliferation, but is debated due to reported misdiagnosed MFs treated with dupilumab with a dramatic progression [34,35,36]. |
IL-5 | Stimulates eosinophilic cascade [37]. | Related to erythroderma and elevated serum levels of IgE. Seems to be overexpressed by CTCL T cells [38]. | AS101 increases IFN-γ and a decreases Il-5, so to affect CTCL progression [24,39]. |
IL-6 | Pro-inflammatory. Differentiates plasma cells and increases adhesion molecule production [40]. | Hyperxpressed in CTCL samples. Seems to be related to a higher risk of MF progression [41,42]. Il-6 polymorphism may be related to worse disease prognosis [43]. | No studies available. |
IL-7 | Hemapoietic factor stimulates the development of lymphoid lineage [44]. | Linked to activation of CD8 + SS clone cells, but studies are not concordant [45,46]. | No studies available. |
IL-8 | IL-8 is a chemotactic factor for neutrophils and other granulocytes. The oncogenic role is achieved by binding the IL-8 R localized on cancer cells and on microenvironment cells [47]. | Involved in pruritus and CTCL progression [48,49]. | No studies available. |
IL-9 | Stimulates various hematopoietic cells’ proliferation and prevents immune cells’ apoptosis. Seems to be related to hematologic neoplasias [50]. | High levels have been linked in patients with SS [51] and MF [52]. | No studies available. |
IL-10 | Anti-inflammatory. Prevention of autoimmune diseases. Can contribute to infection and tumor progression [53,54]. | Higher levels of IL-10 have been detected in MF/SS biopsies compared with normal skin [55,56]. | Vorinostat and romidepsin may exert their therapeutic action due to the downregulation of IL-10 RNA expression [56]. Bortezomib modulates cytokine expression in CTCL, acting on TGFβ1 and IL-10 down-regulation [57]. |
IL-11 | Anti-inflammatory properties. Hematopoiesis, production of platelets from megakaryocytes and hemostasis [58]. | Unknown. | No studies available. |
IL-12 | Activates NK cells and promotes the differentiation of Th1 cells [59]. | Reduces or suppresses IL-12 pathway in CTCL developement, especially in SS patients [60]. | Recombinant IL-12 may restore NK cells functions in CTCLs [61]. |
IL-13 | Anti-inflammatory. Related to Th2 axis [62]. | IL-13 may act as an autocrine factor in lymphoma cell proliferation through IL-13Rα1 and IL-13-Rα2 signaling [63]. A higher expression of IL-13 and its receptors correlates with late stages, while in the early stages, the expression is low [63]. | Dupilumab, by blocking IL-4 and IL-13, could induce an immune system against the tumor and halt Th2 cell proliferation, but this is debated due to reported misdiagnosed MFs treated with dupilumab with a dramatic progression [34,35,36]. |
IL-14 | Growth of B cells. Produced by T cells and certain malignant B cells [64]. | Unknown. | No studies available. |
IL-15 | Enhances CD8 T cell cytotoxic activity, B cell differentiation, Ig synthesis, and DC maturation [65]. | This is implied in the recruitment of CD4+ memory T cells to the skin, induction of T cell proliferation, and inhibition of apoptotic cell death [65,66]. Linked to later stages of CTCL and assumed to promote disease progression [67]. | HDAC inhibitors [68] could halt Zeb1, which leads to an overexpression of IL-15 [69]. |
IL-16 | Pro-inflammatory [70]. | Related to early MF stages [70]. | No studies available. |
IL-17 | Enhances immune response against infectious agents. Upregulates pro-inflammatory cytokines, chemokines, metalloproteinases, and antimicrobial peptides [71]. | Low expression of IL-17 mRNA levels in MF/SS samples compared to healthy donors [66,72]. | No studies available. |
IL-18 | Has a role in adaptive immunity. Induces IFN-γ production [73]. | Higher expression in all MF stages compared to control cases. Role in tumor escape in SS [74]. | No studies available. |
IL-19 | Pro-inflammatory [75]. | IL-19 levels correlated positively with HMGB1, a protein associated with angiogenesis, Th2 polarization, and CTCL progression [76] | No studies available. |
IL-20 | Immunosuppression [75]. | Unknown. | No studies available. |
IL-21 | IL-21 enhances cytotoxicity and induces the production of IFN-γ and perforin by NK cells [77]. | Unknown. | No studies available. |
IL-22 | Immunosuppression [54]. | IL-22 could play a role in establishing the tumor microenvironment in MF [78]. | No studies available. |
IL-23 | Pro-inflammatory [79]. | Unknown. | No studies available. |
IL-24 | Pro-inflammatory [54]. | Unknown. | No studies available. |
IL-25 | Causes Th2 phenotype polarization and IL-4, IL-5, and IL-13 production. It inhibits TH1 and TH17 responses through inhibition of IL-12 and IL-23 [80]. | Higher expression in MF and SS epidermal keratinocytes, compared to controls. IL-25 levels in skin lesions related to disease progression and serum levels correlated with LDH levels [41]. IL-25 enhances IL-13 production by tumor shifting to a Th2 dominant microenvironment [80]. | No studies available. |
IL-26 | Pro-inflammatory [54]. | Unknown. | No studies available. |
IL-27 | IL-27 promotes Th1 immunity, IFN-γ production by NK and T cells, and inhibits Th2 response [81]. | IL-27 levels were higher in advanced stages compared to early stages or controls in MF [81,82]. | No studies available. |
IL-28 | See IFN-γ. | Unknown. | No studies available. |
IL-29 | See IFN-γ. | Unknown. | No studies available. |
IL-30 | Pro-inflammatory [81]. | Unknown. | No studies available. |
IL-31 | Produced by CD4+ Th2 cells, mast cells, and dendritic cells. It modulates fibroblasts and eosinophils. | Increased levels have been detected in both serum and skin lesions [83]. It seems to be related to pruritus, but is still debated [49,84,85]. | No studies available. |
IL-32 | Immunosuppression and cancer progression [30]. | IL-32 is associated with MF development and progression [86]. | No studies available. |
IL-33 | Causes M2 macrophages’ differentiation and induces maturation of dendritic cells [87]. Promotes Th1-mediated responses, including cell-mediated cytotoxicity [88]. | IL-33 might accelerate MF progression via a paracrine action in the tumor microenvironment [89,90]. | No studies available. |
TNF-A | Pro-inflammatory [91]. | TNF–α has been implicated in the development of CTCL by the promotion of epidermotropism via the induction of interferon-inducible protein. TNF-a acts as an autocrine growth factor, enhancing its tumorigenic action and empowering the NF/KB pathway. | No studies available. |
EGF | Epidermal stem cells’ proliferation and differentiation [92]. | Possible role due to its known effect in inhibiting IFN type 1, low levels of which are related to MF development [91]. | No studies available. |
FGF | Mesenchimal stem cells’ proliferation, survival, migration, and differentiation [93]. | FGF’s role has been hypothesized in paraneoplastic scleroderma in MF [93]. | No studies available. |
PDGFR | Varous cellular lines’ growth, proliferation, and differentiation [94]. | Unknown. | No studies available. |
IFN [95,96] | Pro-inflammatory [97,98,99,100]. | The administration of IFN -α is a well-known efficient treatment in advanced-stage CTCLS [96,97,98,99,100,101]. Recombinant IFN-γ a in monotherapy or in association with other therapies, such as phototherapy, bexarotene, vorinostat, and ifn-α, did not provide clear-cut results due to the small sample size of the studies [96,97,98,99,100,101]. |
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Guglielmo, A.; Zengarini, C.; Agostinelli, C.; Motta, G.; Sabattini, E.; Pileri, A. The Role of Cytokines in Cutaneous T Cell Lymphoma: A Focus on the State of the Art and Possible Therapeutic Targets. Cells 2024, 13, 584. https://doi.org/10.3390/cells13070584
Guglielmo A, Zengarini C, Agostinelli C, Motta G, Sabattini E, Pileri A. The Role of Cytokines in Cutaneous T Cell Lymphoma: A Focus on the State of the Art and Possible Therapeutic Targets. Cells. 2024; 13(7):584. https://doi.org/10.3390/cells13070584
Chicago/Turabian StyleGuglielmo, Alba, Corrado Zengarini, Claudio Agostinelli, Giovanna Motta, Elena Sabattini, and Alessandro Pileri. 2024. "The Role of Cytokines in Cutaneous T Cell Lymphoma: A Focus on the State of the Art and Possible Therapeutic Targets" Cells 13, no. 7: 584. https://doi.org/10.3390/cells13070584
APA StyleGuglielmo, A., Zengarini, C., Agostinelli, C., Motta, G., Sabattini, E., & Pileri, A. (2024). The Role of Cytokines in Cutaneous T Cell Lymphoma: A Focus on the State of the Art and Possible Therapeutic Targets. Cells, 13(7), 584. https://doi.org/10.3390/cells13070584