CD4+ T cell differentiation, originally described by Mossman and Coffman resulted in either Th1 or Th2 subsets based on their functional properties. Their groundbreaking findings provided a plausible explanation for previous observations that cellular and humoral immunity were controlled by separate and distinct mechanisms. Subsequent studies on the type 2 inflammatory immune response and its control by CD4+ T cells described a detailed system of interrelated cytokines and transcription factors required to regulate B cell immunoglobulin (Ig) class switching, as well as to mediate the activation of a complex downstream network of innate immune cells. This includes eosinophils, basophils, type 2 innate like cells (ILC2), mast cells and M2 macrophages.
Initially, the role for CD4+ T cells in regulating and directing type 2 immune responses was described in relation to Th2 differentiation that controls the induction of asthma and allergic responses on one side of the coin and control of anti-parasitic responses on the other. Recently, several new areas of research interest have explored CD4+ T cell control of type 2 immune associated responses for maintaining homeostasis and protecting against onset of metabolic syndrome/type 2 diabetes and supporting muscle regeneration or wound repair. Moreover, novel CD4+ T cell subsets and specialized innate cells that participate in type 2 immune responses as contributing to type II inflammation have been identified and characterized, including Tfh, Th9, ILC2 and M2 macrophages, among others. The role of CD4+ T cells in the production of the canonical Th2 associated cytokines, has yet to be adequately settled with the description of IL4/IL13 production by Tfh and the observation of a potential spatial and functional separation of IL4 and IL13 producers during the immune response. As such, the role of Th2 cytokine-producing CD4+ T cell as an immune contributor to type 2 inflammation continues to evolve both in terms of their functional properties and also in relation to the diseases and tissues in which they play a key role, under both homeostatic and inflammatory conditions.
In this Research Topic, we aim to present Original Research, Review and Perspective articles dedicated to the latest advances in research on the role of CD4+ T cells in regulating the type II inflammatory response. Areas to be covered may include:
- Novel roles for CD4+ T cell responses in disease pathogenesis
- CD4+ T cells in the control of homeostasis and the role of type II inflammation in the prevention of type 2 diabetes and metabolic disease
-Type II inflammatory responses in protection against muscle damage and in wound healing
- New insights into T helper subset differentiation, definitions and implications for type II inflammatory responses
-Innate immune cell interactions with CD4+ T cells
- Signaling pathways and T cell differentiation or innate immune cell activation in the context of the type II inflammatory response
CD4+ T cell differentiation, originally described by Mossman and Coffman resulted in either Th1 or Th2 subsets based on their functional properties. Their groundbreaking findings provided a plausible explanation for previous observations that cellular and humoral immunity were controlled by separate and distinct mechanisms. Subsequent studies on the type 2 inflammatory immune response and its control by CD4+ T cells described a detailed system of interrelated cytokines and transcription factors required to regulate B cell immunoglobulin (Ig) class switching, as well as to mediate the activation of a complex downstream network of innate immune cells. This includes eosinophils, basophils, type 2 innate like cells (ILC2), mast cells and M2 macrophages.
Initially, the role for CD4+ T cells in regulating and directing type 2 immune responses was described in relation to Th2 differentiation that controls the induction of asthma and allergic responses on one side of the coin and control of anti-parasitic responses on the other. Recently, several new areas of research interest have explored CD4+ T cell control of type 2 immune associated responses for maintaining homeostasis and protecting against onset of metabolic syndrome/type 2 diabetes and supporting muscle regeneration or wound repair. Moreover, novel CD4+ T cell subsets and specialized innate cells that participate in type 2 immune responses as contributing to type II inflammation have been identified and characterized, including Tfh, Th9, ILC2 and M2 macrophages, among others. The role of CD4+ T cells in the production of the canonical Th2 associated cytokines, has yet to be adequately settled with the description of IL4/IL13 production by Tfh and the observation of a potential spatial and functional separation of IL4 and IL13 producers during the immune response. As such, the role of Th2 cytokine-producing CD4+ T cell as an immune contributor to type 2 inflammation continues to evolve both in terms of their functional properties and also in relation to the diseases and tissues in which they play a key role, under both homeostatic and inflammatory conditions.
In this Research Topic, we aim to present Original Research, Review and Perspective articles dedicated to the latest advances in research on the role of CD4+ T cells in regulating the type II inflammatory response. Areas to be covered may include:
- Novel roles for CD4+ T cell responses in disease pathogenesis
- CD4+ T cells in the control of homeostasis and the role of type II inflammation in the prevention of type 2 diabetes and metabolic disease
-Type II inflammatory responses in protection against muscle damage and in wound healing
- New insights into T helper subset differentiation, definitions and implications for type II inflammatory responses
-Innate immune cell interactions with CD4+ T cells
- Signaling pathways and T cell differentiation or innate immune cell activation in the context of the type II inflammatory response
