Transforming growth factor-beta (TGF-beta) is a potent regulatory cytokine with diverse effects on hemopoietic cells. The pivotal function of TGF-beta in the immune system is to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival. In addition, TGF-beta controls the initiation and resolution of inflammatory responses through the regulation of chemotaxis, activation, and survival of lymphocytes, natural killer cells, dendritic cells, macrophages, mast cells, and granulocytes. The regulatory activity of TGF-beta is modulated by the cell differentiation state and by the presence of inflammatory cytokines and costimulatory molecules. Collectively, TGF-beta inhibits the development of immunopathology to self or nonharmful antigens without compromising immune responses to pathogens. This review highlights the findings that have advanced our understanding of TGF-beta in the immune system and in disease.

Transforming growth factor-beta regulation of immune responses.

Allogeneic haematopoietic stem-cell transplantation (SCT) is a curative therapy for haematological malignancies and inherited disorders of blood cells, such as sickle-cell anaemia. Mature alphabeta T cells that are contained in the allografts reconstitute T-cell immunity and can eradicate malignant cells in the recipient. Unfortunately, these T cells recognize the recipient as 'non-self' and employ a wide range of immune mechanisms to attack recipient tissues in a process known as graft-versus-host disease (GVHD). The full therapeutic potential of allogeneic haematopoietic SCT will not be realized until approaches to minimize GVHD, while maintaining the positive contributions of donor T cells, are developed. This Review focuses on research in mouse models pursued to achieve this goal.

Graft-versus-host disease.

Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes

T cell subsets and their signature cytokines in autoimmune and inflammatory diseases

Typical immune responses lead to prominent clonal expansion of antigen-specific T and B cells followed by differentiation into effector cells. Most effector cells die at the end of the immune response but some of these cells survive and form long-lived memory cells. The factors controlling the formation and survival of memory T cells are reviewed.

T Cell Memory

The effector cytokine interferon γ (IFN-γ) may play a role in T cell homeostasis. We have examined the requirement for IFN-γ in one mechanism that regulates T cell expansion and survival, activation-induced cell death (AICD). CD4+ T cells lacking IFN-γ or the Stat1 transcription factor are resistant to AICD. IFN-γ is required for the production of caspases, and retrovirus-mediated expression of caspase-8 restores the sensitivity of Stat1-deficient T cells to AICD. In vitro, IFN-γ limits the expansion of T cells that are stimulated through their antigen receptors. Thus, IFN-γ may function to control the expansion and persistence of T cells by promoting caspase-8–dependent apoptosis.

/pdf/interferon-g-is-required-for-activation-induced-death-of-t-2zhnesmf61.pdf

Interferon γ Is Required for Activation-induced Death of T Lymphocytes

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Interferon γ Is Required for Activation-induced Death of T Lymphocytes