Community Series in the Role of CD1- and MR1-restricted T cells in Immunity and Disease, volume II

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87

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18

articles

Community Series in the Role of CD1- and MR1-restricted T cells in Immunity and Disease, volume II

57.1K

views

87

authors

18

articles

Editorial

16 September 2024

Editorial: Community series in the role of CD1- and MR1-restricted T cells in immunity and disease, volume II

Kazuya Iwabuchi

and

Luc Van Kaer

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Editors

2

Vanderbilt University Medical Center

Kazuya Iwabuchi

Department of Immunology, Kitasato University School of Medicine

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This is the second volume in the series, the Role of CD1- and MR1-restricted T cells in Immunity and Disease. Please see volume I here.

CD1 and MR1 are major histocompatibility complex (MHC) class I-related proteins that bind and present non-peptide antigens to subsets of T cells with specialized functions. CD1 proteins typically present lipid antigens to CD1-restricted T cells, whereas MR1 presents vitamin B-based ligands and a variety of drugs and drug-like molecules to MR1-restricted T cells.

The CD1 family of antigen-presenting molecules has been divided into two groups: Group 1 contains CD1a, CD1b, and CD1c, and Group 2 contains CD1d. Additionally, CD1e is expressed intracellularly and is involved in the loading of lipid antigens onto Group 1 CD1 proteins. Humans express both Groups 1 and 2 CD1 proteins, whereas mice only express CD1d. Group 1 CD1 proteins present lipid antigens to T cells that generally express diverse T cell receptors (TCRs) and exhibit adaptive-like functions, whereas CD1d presents lipid antigens to subsets of T cells that express either diverse or highly restricted TCRs and exhibit innate-like functions. CD1d-restricted T cells are called natural killer T (NKT) cells, which include Type I or invariant NKT (iNKT) cells expressing semi-invariant TCRs, and Type II NKT cells expressing more diverse TCRs. CD1-restricted T cells have been implicated in a wide variety of diseases, including cancer, infections, and autoimmune, inflammatory, and metabolic diseases. Additionally, NKT cells have been targeted for immunotherapy of disease with ligands such as ?a or a-galactosylceramide for iNKT cells, or sulfatide for Type II NKT cells.

Like iNKT cells, most MR1-restricted T cells, often called mucosal-associated invariant T (MAIT) cells, express semi-invariant TCRs and display innate-like functions. MAIT cells have been implicated in immune responses against a variety of pathogens such as Mycobacterium tuberculosis, Pseudomonas aeruginosa, Helicobacter pylori, hepatitis C virus, and influenza virus. Moreover, these cells contribute to autoimmune and inflammatory diseases, including colitis, rheumatoid arthritis, psoriasis, lupus, and diabetes.

In this Research Topic, we welcome the submission of Review, Mini Review, Original Research, Brief Research Report, Perspective, General Commentary, and Opinion articles on the contribution of CD1- and MR1-restricted T cells to microbial infections, cancer, autoimmunity, and a broad spectrum of inflammatory diseases, including, but not limited to, colitis, airway hypersensitivity, hepatitis, atherosclerosis, and the metabolic syndrome. Articles that focus predominantly on disease prophylaxis or immunotherapy are also welcome to be submitted to this Research Topic.

This is the second volume in the series, the Role of CD1- and MR1-restricted T cells in Immunity and Disease. Please see volume I here.

CD1 and MR1 are major histocompatibility complex (MHC) class I-related proteins that bind and present non-peptide antigens to subsets of T cells with specialized functions. CD1 proteins typically present lipid antigens to CD1-restricted T cells, whereas MR1 presents vitamin B-based ligands and a variety of drugs and drug-like molecules to MR1-restricted T cells.

The CD1 family of antigen-presenting molecules has been divided into two groups: Group 1 contains CD1a, CD1b, and CD1c, and Group 2 contains CD1d. Additionally, CD1e is expressed intracellularly and is involved in the loading of lipid antigens onto Group 1 CD1 proteins. Humans express both Groups 1 and 2 CD1 proteins, whereas mice only express CD1d. Group 1 CD1 proteins present lipid antigens to T cells that generally express diverse T cell receptors (TCRs) and exhibit adaptive-like functions, whereas CD1d presents lipid antigens to subsets of T cells that express either diverse or highly restricted TCRs and exhibit innate-like functions. CD1d-restricted T cells are called natural killer T (NKT) cells, which include Type I or invariant NKT (iNKT) cells expressing semi-invariant TCRs, and Type II NKT cells expressing more diverse TCRs. CD1-restricted T cells have been implicated in a wide variety of diseases, including cancer, infections, and autoimmune, inflammatory, and metabolic diseases. Additionally, NKT cells have been targeted for immunotherapy of disease with ligands such as ?a or a-galactosylceramide for iNKT cells, or sulfatide for Type II NKT cells.

Like iNKT cells, most MR1-restricted T cells, often called mucosal-associated invariant T (MAIT) cells, express semi-invariant TCRs and display innate-like functions. MAIT cells have been implicated in immune responses against a variety of pathogens such as Mycobacterium tuberculosis, Pseudomonas aeruginosa, Helicobacter pylori, hepatitis C virus, and influenza virus. Moreover, these cells contribute to autoimmune and inflammatory diseases, including colitis, rheumatoid arthritis, psoriasis, lupus, and diabetes.

In this Research Topic, we welcome the submission of Review, Mini Review, Original Research, Brief Research Report, Perspective, General Commentary, and Opinion articles on the contribution of CD1- and MR1-restricted T cells to microbial infections, cancer, autoimmunity, and a broad spectrum of inflammatory diseases, including, but not limited to, colitis, airway hypersensitivity, hepatitis, atherosclerosis, and the metabolic syndrome. Articles that focus predominantly on disease prophylaxis or immunotherapy are also welcome to be submitted to this Research Topic.

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Editors

Vanderbilt University Medical Center

Kazuya Iwabuchi

Department of Immunology, Kitasato University School of Medicine

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