Table 1.
Section | Cell type | Proposed roles in allergy | Proposed functions in cancer |
---|---|---|---|
3.1 | Dendritic cells | Support conversion of T cells into Tregs | Depending on differentiation; Support conversion of T cells into immunosuppressive Tregs, promoting cancer progression |
3.2 | Macrophages | M2a macrophages support allergic diseases M2b have immunoregulatory functions |
Depending on subtype; M1 macrophages support survival Low M1/M2 ratios associated with poor survival M2b associated with tolerogenic tumour microenvironment |
3.3 | Tregs | Source of IL-10, supported by IL-10 Foster IgG4 production and suppress allergies |
Accumulate in cancer tissue Correlate with disease progression |
3.4 | Bregs | Source and recipient of IL-10 Origin of IgG4 in allergen immunotherapy |
Source and recipient of IL-10 Origin of IgG4 in cancer tissues, where they correlate with disease severity and poorer outcomes |
3.5 | Innate lymphoid cells (ILCs) | Source of Th2 cytokines and thus involved in initiation of allergy | Depending on subtype; ILC2 may in a tumour provide an immunosuppressive environment, like ILC3s which support IL-10 secretion |
3.6 | Mast cells | Major effector cells in allergy and source of IL-4 | Controversial; Can engender pro- or anti-tumoural functions, depending on micro-localization and type of tumour A source of TNFα; Can express PD-L1 or -L2 and inhibit effector T cells. |
3.7 | Eosinophils | Involved in chronic allergic and atopic conditions and associated with curative processes | Controversial; Attracted by CCL1 in tumour; Can be pro- (Hodgkin´s lymphoma) or anti-tumorigenic (in solid tumours); May sense tumour cells in innate manner and kill in concert with Igs; May induce Tregs |
3.8 | Epithelial cells | Contribute to site-specific tolerance induction, mainly via DC interactions; Epithelial barrier disruption stimulates allergen entry and epithelial activation; Source of TSLP and IL-33, supporting Th2 responses |
Source of immunosuppressive microvesicles, with a potential role in cancer promotion |