Modulating the immune system holds great promise for treating a variety of autoimmune and inflammatory diseases, by stimulating desired immune responses and/or inhibiting undesired immune responses. Traditional methods that exert global suppressive effects on immune responses often impair overall immune competence, as they quell both pathogenic and protective immune responses. More recently developed biological therapies selectively suppress the pathogenic responses in autoimmune and inflammatory diseases by acting on specific cell subsets or molecules. The latter treatments have been developed on the basis of a thorough understanding of the underlying disease pathology, especially the role of antigen-specific effector B and T lymphocytes of the adaptive immune system. However, comparatively little attention has been paid to the immunotherapeutic potential of innate and innate-like effector lymphocytes, which also make important contributions to the development and progression of autoimmune and inflammatory diseases.
The overall goal of this Research Topic is to discuss our emerging understanding of the roles of innate and innate-like lymphocytes in the pathogenesis of autoimmune and inflammatory diseases, and how this information could be exploited for the development of new immunotherapies. Innate and innate-like lymphocytes share a number of features that make them attractive targets for immunotherapy. For example, their specificity is not impacted by polymorphic HLA ligands and, therefore, uniform tools could be employed to elicit their therapeutic properties in genetically disparate individuals. Furthermore, their therapeutic activation or inactivation may not lead to widespread immune impairment and susceptibility to infection.
Submissions may focus on, but don’t need to be limited to, the following subsets of effector innate or innate-like lymphocytes: natural killer (NK) cells, innate lymphoid cells (ILCs), innate intraepithelial lymphocytes (IELs), CD1d-restricted natural killer T (NKT) cells, MR1-restricted mucosal-associated invariant T (MAIT) cells, Qa-1/HLA-E-restricted T cells, H2-M3-restricted T cells, innate subsets of T cell receptor (TCR) γδ-expressing T cells, subsets of innate-like TCR-expressing IELs, conventional antigen-inexperienced T cells with a memory phenotype referred to as innate or virtual memory T cells, marginal zone B (MZB) cells, and B-1 B cells. Articles should focus on the contributions of these cells to the development and/or progression of inflammatory diseases that are caused by autoimmunity, environmental antigens, microbes, cancer, acute or chronic tissue damage, nutrients, or metabolites. A specific effort should be made to discuss how these cells contribute to available immunotherapies or may be targeted for the development of new immunotherapies, either by stimulating, deviating or inhibiting their effector functions. Animal models and/or human studies may be included.
We welcome the submission of Review, Mini Review, Opinion, Perspective, General Commentary and Original Research Articles.
Modulating the immune system holds great promise for treating a variety of autoimmune and inflammatory diseases, by stimulating desired immune responses and/or inhibiting undesired immune responses. Traditional methods that exert global suppressive effects on immune responses often impair overall immune competence, as they quell both pathogenic and protective immune responses. More recently developed biological therapies selectively suppress the pathogenic responses in autoimmune and inflammatory diseases by acting on specific cell subsets or molecules. The latter treatments have been developed on the basis of a thorough understanding of the underlying disease pathology, especially the role of antigen-specific effector B and T lymphocytes of the adaptive immune system. However, comparatively little attention has been paid to the immunotherapeutic potential of innate and innate-like effector lymphocytes, which also make important contributions to the development and progression of autoimmune and inflammatory diseases.
The overall goal of this Research Topic is to discuss our emerging understanding of the roles of innate and innate-like lymphocytes in the pathogenesis of autoimmune and inflammatory diseases, and how this information could be exploited for the development of new immunotherapies. Innate and innate-like lymphocytes share a number of features that make them attractive targets for immunotherapy. For example, their specificity is not impacted by polymorphic HLA ligands and, therefore, uniform tools could be employed to elicit their therapeutic properties in genetically disparate individuals. Furthermore, their therapeutic activation or inactivation may not lead to widespread immune impairment and susceptibility to infection.
Submissions may focus on, but don’t need to be limited to, the following subsets of effector innate or innate-like lymphocytes: natural killer (NK) cells, innate lymphoid cells (ILCs), innate intraepithelial lymphocytes (IELs), CD1d-restricted natural killer T (NKT) cells, MR1-restricted mucosal-associated invariant T (MAIT) cells, Qa-1/HLA-E-restricted T cells, H2-M3-restricted T cells, innate subsets of T cell receptor (TCR) γδ-expressing T cells, subsets of innate-like TCR-expressing IELs, conventional antigen-inexperienced T cells with a memory phenotype referred to as innate or virtual memory T cells, marginal zone B (MZB) cells, and B-1 B cells. Articles should focus on the contributions of these cells to the development and/or progression of inflammatory diseases that are caused by autoimmunity, environmental antigens, microbes, cancer, acute or chronic tissue damage, nutrients, or metabolites. A specific effort should be made to discuss how these cells contribute to available immunotherapies or may be targeted for the development of new immunotherapies, either by stimulating, deviating or inhibiting their effector functions. Animal models and/or human studies may be included.
We welcome the submission of Review, Mini Review, Opinion, Perspective, General Commentary and Original Research Articles.