MeSH

LYMPHOCYTE ACTIVATION by a specific ANTIGEN thus triggering clonal expansion of LYMPHOCYTES already capable of mounting an immune response to the antigen.

Year introduced: 2012

Expansion of blood cells arising from mutant HEMATOPOIETIC STEM CELLS often related to aging. Mutations on epigenetic regulator genes are common in clonal hematopoiesis and may be a risk factor for HEMATOLOGIC NEOPLASMS and other cardiovascular diseases. When variant allele fraction is at least 2% and is present in the absence of severe cytopenias it is referred to as clonal hematopoiesis of indeterminate potential (CHIP).

Year introduced: 2021

The process of accumulation of genetic and epigenetic changes over time in individual cells and the effect of the changes on CELL PROLIFERATION.

Year introduced: 2012

Removal, via CELL DEATH, of immature lymphocytes that interact with antigens during maturation. For T-lymphocytes this occurs in the thymus and ensures that mature T-lymphocytes are self tolerant. B-lymphocytes may also undergo clonal deletion.

Year introduced: 1994

Functional inactivation of T- or B-lymphocytes rendering them incapable of eliciting an immune response to antigen. This occurs through different mechanisms in the two kinds of lymphocytes and can contribute to SELF TOLERANCE.

Year introduced: 1994

A clinically and genetically heterogeneous group of mast cell disorders in which there is aberrant release of mast cell mediators with little to no accompanying proliferation of MAST CELLS.

Year introduced: 2022

The mechanism, in central lymphoid organs (THYMUS; BONE MARROW), that prevents immature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished by CLONAL ANERGY and CLONAL DELETION.

Year introduced: 2012

The mechanism, in peripheral lymphoid organs (LYMPH NODES; SPLEEN; TONSILS; and mucosal-associated lymphoid tissue), that prevents mature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished through a variety of means including CLONAL ANERGY and CLONAL DELETION.

Year introduced: 2012

The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.

Year introduced: 1994

A family of receptors that modulate the activation of T-LYMPHOCYTES by the T-CELL ANTIGEN RECEPTOR. The receptors are responsive to one or more B7 ANTIGENS found on ANTIGEN-PRESENTING CELLS and, depending upon the specific ligand-receptor combination, modulate a variety of T-cell functions such as the rate of clonal expansion, CELL SURVIVAL and cytokine production. Although commonly referred to as costimulatory receptors, some of the receptors have inhibitory effects such as inducing PERIPHERAL TOLERANCE.

Year introduced: 2012

Clonal myeloid disorders that possess both dysplastic and proliferative features but are not properly classified as either MYELODYSPLASTIC SYNDROMES or MYELOPROLIFERATIVE DISORDERS.

Year introduced: 2008

A spectrum of disorders characterized by clonal expansions of the peripheral blood LYMPHOCYTE populations known as large granular lymphocytes which contain abundant cytoplasm and azurophilic granules. Subtypes develop from either CD3-negative NATURAL KILLER CELLS or CD3-positive T-CELLS. The clinical course of both subtypes can vary from spontaneous regression to progressive, malignant disease.

Year introduced: 2008

A continuous cell line that is a substrain of SWISS 3T3 CELLS developed though clonal isolation. The mouse fibroblast cells undergo an adipose-like conversion as they move to a confluent and contact-inhibited state.

Year introduced: 2004

Microbial antigens that have in common an extremely potent activating effect on T-cells that bear a specific variable region. Superantigens cross-link the variable region with class II MHC proteins regardless of the peptide binding in the T-cell receptor's pocket. The result is a transient expansion and subsequent death and anergy of the T-cells with the appropriate variable regions.

Year introduced: 1994

A group of lymphomas exhibiting clonal expansion of malignant T-lymphocytes arrested at varying stages of differentiation as well as malignant infiltration of the skin. MYCOSIS FUNGOIDES; SEZARY SYNDROME; LYMPHOMATOID PAPULOSIS; and PRIMARY CUTANEOUS ANAPLASTIC LARGE CELL LYMPHOMA are the best characterized of these disorders.

Year introduced: 1991

Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.

Year introduced: 2008 (1989)

Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.

Year introduced: 2008 (1989)

Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.

Year introduced: 1986

A rare neoplastic disorder characterized by a clonal proliferation of MAST CELLS, associated with KIT-D816 mutations, and accompanied by aberrant mast cell activation. The abnormal increase of MAST CELLS may occur in only the skin (MASTOCYTOSIS, CUTANEOUS), in extracutaneous tissues involving multiple organs (MASTOCYTOSIS, SYSTEMIC), or in solid tumors (MASTOCYTOMA).

Year introduced: 1987

A multilineage cell growth factor secreted by LYMPHOCYTES; EPITHELIAL CELLS; and ASTROCYTES which stimulates clonal proliferation and differentiation of various types of blood and tissue cells.

Year introduced: 1987