Skip to main content
. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Allergy. 2017 Oct 5;73(2):328–340. doi: 10.1111/all.13311

Table 1.

Cellular players in immune tolerance in allergy and cancer.

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