Immunology Terms Starting With D

DAMPs are endogenous molecules released from damaged or dying cells that activate innate immune pattern recognition receptors, signaling tissue injury or cellular stress in the absence of infection.

DAMPs include intracellular molecules such as ATP, HMGB1 protein, heat shock proteins, and uric acid crystals that normally reside inside healthy cells but are released during necrosis, trauma, or ischemic injury. Unlike PAMPs derived from pathogens, DAMPs originate from the host itself and trigger sterile inflammation through pattern recognition receptors including Toll-like receptors and NOD-like receptors. HMGB1, one of the best-studied DAMPs, can rise up to 1,000-fold in concentration in inflamed tissues and activate multiple immune pathways.

Chronic DAMP release contributes to diseases such as atherosclerosis and Alzheimer’s disease, where sterile inflammation damages tissues without any microbial trigger.

Defensin is a small cationic antimicrobial peptide produced by immune cells and epithelial tissues that kills bacteria, fungi, and enveloped viruses by forming pores in microbial membranes as part of the innate immune response.

Defensins are typically 18 to 45 amino acids long and contain three intramolecular disulfide bonds that stabilize their characteristic beta-sheet structure. Humans produce two main families: alpha-defensins, concentrated in neutrophil granules and Paneth cells of the small intestine, and beta-defensins, secreted by epithelial cells throughout the respiratory, urogenital, and gastrointestinal tracts. Human neutrophils store approximately 3 milligrams of alpha-defensins per 10 million cells, representing up to 50 percent of total granule protein.

Beyond direct membrane disruption, defensins recruit dendritic cells and T cells to infection sites and can neutralize bacterial lipopolysaccharide, bridging innate and adaptive immunity.

Delayed Hypersensitivity is an immune reaction mediated by sensitized T cells rather than antibodies that develops 24 to 72 hours after antigen contact, producing tissue inflammation through cytokine release and macrophage activation.

When a sensitized individual re-encounters the antigen, antigen-presenting cells display processed peptides to memory CD4 T cells, which secrete IFN-gamma and TNF that recruit and activate macrophages at the site. This cellular infiltration produces the characteristic induration and erythema that peaks one to three days after exposure. The tuberculin skin test exploits this reaction to detect prior exposure to Mycobacterium tuberculosis: a raised, firm wheal of 10 millimeters or more at 48 to 72 hours is considered a positive result.

Allergic contact dermatitis from nickel, poison ivy (Toxicodendron radicans), or latex follows the same T cell-driven mechanism and can persist for days after the offending antigen is removed.

Dendritic Cell is a professional antigen-presenting cell with branching cytoplasmic projections that samples antigens in peripheral tissues, matures upon pathogen detection, and migrates to lymph nodes to activate naive T and B lymphocytes.

Immature dendritic cells in tissues continuously endocytose and process antigens from their surroundings. Detection of pathogen-associated molecular patterns through Toll-like receptors and other innate sensors triggers maturation, during which the cells upregulate MHC class II, co-stimulatory molecules CD80 and CD86, and CCR7, the chemokine receptor that guides migration toward lymph nodes. Plasmacytoid dendritic cells are a specialized subset that produces large quantities of type I interferons in response to viral nucleic acids, releasing up to 1,000 times more IFN-alpha than other cell types.

Ralph Steinman, who discovered dendritic cells in 1973, received the Nobel Prize in Physiology or Medicine in 2011 for demonstrating their central role in adaptive immunity.