Immunology Terms Starting With T

T Cell is a lymphocyte that matures in the thymus and mediates cellular adaptive immunity through helper, cytotoxic, and regulatory subsets that coordinate and execute immune responses against infected, cancerous, and foreign cells.

T cells express unique T cell receptors generated by somatic V(D)J recombination that recognize short peptide fragments bound to MHC molecules on the surface of antigen-presenting or target cells. Thymic development imposes two sequential selection checkpoints: positive selection retains only cells whose receptors can recognize self-MHC, while negative selection eliminates cells whose receptors bind self-peptide-MHC with dangerously high affinity, together producing a mature repertoire tolerant of self yet capable of responding to foreign antigens. CD4-positive helper T cells recognize peptides on MHC class II and coordinate responses by secreting cytokines, whereas CD8-positive cytotoxic T cells recognize peptides on MHC class I and kill infected or malignant cells directly.

Estimates suggest the human naive T cell repertoire contains between 25 million and 100 million distinct receptor specificities, providing broad coverage against novel pathogens.

T Lymphocyte is a white blood cell of the adaptive immune system that matures in the thymus, expresses an antigen-specific T cell receptor, and mediates cellular immune responses including direct cytotoxic killing of infected or malignant cells.

T lymphocytes and B lymphocytes together constitute the adaptive immune system, with T cells providing the cellular arm and B cells providing the humoral arm through antibody production. During thymic education, developing T lymphocytes undergo positive selection for MHC recognition and negative selection to eliminate self-reactive clones, a process so stringent that roughly 98 percent of all thymocytes die before reaching maturity. Functional diversity among T lymphocytes spans cytotoxic CD8-positive killers, CD4-positive helper coordinators, and Foxp3-expressing regulatory suppressors, each distinguished by surface markers, cytokine profiles, and target cell interactions.

A single naive T lymphocyte that encounters its cognate antigen can expand into a clone of thousands of effector cells within five to seven days, then contract to a small pool of long-lived memory cells after the threat is cleared.

Thymus is a primary lymphoid organ in the anterior chest that provides the microenvironment for T cell maturation, positive selection for MHC recognition, and negative selection to eliminate self-reactive T cells.

T cell precursors migrate from bone marrow to the thymic cortex, where they rearrange TCR genes and undergo positive selection by cortical thymic epithelial cells presenting self-peptide-MHC complexes. Cells that cannot recognize self-MHC die by neglect, while cells that bind too strongly to self-antigens are removed during negative selection in the medulla. Medullary thymic epithelial cells use the AIRE gene to express tissue-restricted antigens, allowing developing T cells to be tested against proteins normally found in organs such as the pancreas, thyroid, and skin.

The thymus is largest relative to body size in infancy and then involutes after puberty, progressively reducing naive T cell output with age.

Toll-Like Receptor is a pattern recognition receptor of the innate immune system that detects conserved microbial or damage-associated molecular patterns such as bacterial lipopolysaccharide, flagellin, viral RNA, or unmethylated microbial DNA.

Humans have 10 Toll-like receptor family members, expressed either on cell surfaces or in endosomal membranes, with well-characterized microbial ligands for most but not all members. TLR4 detects lipopolysaccharide from gram-negative bacteria, TLR2 recognizes bacterial lipoproteins, TLR5 binds flagellin, and TLR3, TLR7, TLR8, and TLR9 detect microbial nucleic acids in endosomal compartments. TLR signaling through MyD88 and TRIF adaptor proteins activates transcription factors including NF-kappaB and IRF3, producing pro-inflammatory cytokines and type I interferons.

TLR10 is unusual because its ligand biology and signaling role are less settled than those of other human TLRs, and several studies suggest it may have modulatory or inhibitory functions. The TLR family was first linked to immunity through Drosophila melanogaster Toll signaling, showing that pattern-recognition pathways predate vertebrate adaptive immunity.

TTC37 is a gene encoding a tetratricopeptide repeat-containing scaffold protein of the cytoplasmic SKI complex that directs aberrant RNAs to the exosome for degradation, and whose loss-of-function mutations cause trichohepatoenteric syndrome, a rare disorder combining intractable diarrhea, liver disease, woolly hair, and immune deficiency.

TTC37 encodes the human ortholog of yeast Ski3, a scaffold subunit that assembles the trimeric SKI complex together with SKIV2L and WDR61. This complex threads aberrant cytoplasmic RNAs, including non-stop and no-go decay substrates, into the exosome for 3-prime-to-5-prime degradation. When TTC37 is non-functional, unprocessed RNA species accumulate and activate innate RNA-sensing pathways, producing chronic type I interferon signaling and intestinal inflammation that mirrors the phenotype caused by SKIV2L mutations.

Trichohepatoenteric syndrome caused by TTC37 mutations was genetically defined in 2012 by Fabre and colleagues, who identified biallelic mutations in a cohort of patients from multiple countries, establishing RNA quality control as a mechanism of monogenic inflammatory bowel disease.

Tumor Necrosis Factor is a pro-inflammatory cytokine produced mainly by macrophages and T cells that mediates acute-phase responses, activates endothelium, promotes neutrophil recruitment, and in chronic excess drives pathological inflammation.

Tumor necrosis factor alpha binds TNFR1 on many nucleated cells, recruiting adaptor protein TRADD and activating both pro-survival NF-kappaB signaling through RIPK1 and pro-death caspase-8 signaling depending on cellular context. TNF produced by macrophages stimulates endothelial cells to upregulate adhesion molecules, allowing neutrophils and monocytes to exit the bloodstream and enter infected tissue. In tuberculosis, TNF helps maintain granulomas that wall off Mycobacterium tuberculosis, which explains why TNF inhibitor therapy can increase the risk of reactivating latent tuberculosis if screening and preventive treatment are not performed.

Therapeutic TNF blockade with monoclonal antibodies or receptor fusion proteins has transformed rheumatoid arthritis, inflammatory bowel disease, and psoriasis by suppressing chronic inflammatory signaling.