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DEFINITIONS

  • Anergy—A reversible tolerance mechanism in which the T or B cell is in an unresponsive state following an antigen encounter but remains alive.

  • Chimeric antigen receptor T cells (CAR T)—Synthetic hybrid receptors created by recombinant techniques that combine an extracellular domain, usually derived from an antibody single-chain variable fragment (scFv), with intracellular signaling domains from activating co-stimulatory molecules (from endogenous T-cell receptors [TCRs], CD28, or 4-1BB) that allow for retargeting of T cells to antigens on malignant cells.

  • Checkpoint inhibition therapy—A form of cancer immunotherapy whereby antibodies against T-cell or antigen-presenting cell regulators of immune cell inhibition are used to activate cytotoxic T cells to kill tumor cells.

  • Co-stimulation of T cells—A secondary signal that T cells require for activation following presentation of peptide antigen by major histocompatibility complex (MHC) molecules to TCRs on either CD4 or CD8 T cells. A prime mediator of co-stimulation is the T cell CD28 molecule binding to B7-1 (CD80, CD86) on antigen-presenting cells.

  • Cytokines—Soluble proteins that interact with specific cellular receptors that are involved in the regulation of the growth and activation of immune cells and mediate normal and pathologic inflammatory and immune responses.

  • Immune homeostasis—Balanced protective immunity that does not overreact to pathogens and harm the host, and immunity that is not deficient and does not predispose the host to harmful infections or malignancies.

  • Immunoediting—Process of immunity selecting clones of cancer cells with reduced immunogenicities resulting in tumor escape.

  • Natural killer cells—Lymphocytes with cytotoxic potential for host cells with non-self-antigens, such as cells infected with pathogens or tumor cells expressing tumor-specific neoantigens.

  • T-cell exhaustion—State of T cells when the persistence of antigen disrupts memory T-cell function, resulting in defects in memory T-cell responses. Most frequently occurs in malignancies and in chronic viral infections such as HIV-1 and hepatitis C.

  • T regulatory cells (Tregs)—CD4 and CD8 T cells regulated by the transcription factor FOXP3 that play roles in downmodulating B- and T-cell responses in peripheral lymphoid tissues to prevent deleterious immune activation that can lead to autoimmune diseases.

  • Tumor-infiltrating lymphocytes—Lymphocytes that infiltrate tumors that may be in the exhausted state and upon which checkpoint inhibition therapy works.

  • Tumor neoantigens—Molecules in malignant cells that develop mutations that create non-self-antigens that are recognized by host T cells as non-self and against which tumor-infiltrating CD4 and CD8 T cells respond to reject the tumor.

INTRODUCTION

Immune homeostasis is the maintenance of a balance between immunity that protects the host and dysregulated immunity that predisposes the host to harmful infections, autoimmunity, or malignancies. Overactivity of innate and adaptive immunity leads to autoimmunity and/or inflammatory diseases. Underactivity of immune responses can lead to both immune deficiency and autoimmunity. Disruption of immune homeostasis contributes either directly or indirectly to many forms of disease. Thus, a major goal of immunotherapy is to either maintain immune homeostasis or reestablish immune balance in diseases of ...

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