Puzzle 03: Immunity, Inflammation, and Hypersensitivity

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Across
  1. 3. A specialized family of low-molecular-weight cytokines that primarily function to recruit specific leukocyte populations to sites of inflammation.
  2. 5. Sulfur-containing lipid mediators derived from arachidonic acid that induce prolonged bronchoconstriction and vascular permeability changes.
  3. 7. The immediate cellular process where mast cells release preformed biochemical mediators like histamine into the extracellular space.
  4. 8. The genetic complex (MHC/HLA) that codes for cell-surface proteins used by the immune system to distinguish self from non-self.
  5. 11. A specialized family of signaling cytokines released by virally infected host cells to alert neighboring cells and induce antiviral defense mechanisms.
  6. 12. A severe, systemic Type I hypersensitivity reaction characterized by widespread vasodilation, airway constriction, and systemic shock.
  7. 14. A critical class of cytokines produced primarily by macrophages and lymphocytes to regulate immune responses and leukocyte cross-talk.
  8. 15. The immunological process where pathogens are coated with antibodies or complement fragments (like C3b) to tag them for phagocytosis.
  9. 21. The directional migration of white blood cells along a chemical concentration gradient toward the site of tissue injury.
  10. 22. An advanced inflammatory exudate that is thick and sticky, containing large amounts of clotting proteins, typically seen in severe pericarditis.
  11. 23. A breakdown in immunological self-tolerance where the body's immune system mistakenly attacks its own healthy tissues and organs.
  12. 26. A specialized focal wall of macrophages, epithelioid cells, and lymphocytes formed to sequester indigestible foreign material or pathogens.
  13. 29. An inflammatory fluid containing high concentrations of protein and cellular debris that escapes from blood vessels into surrounding tissues.
  14. 30. An altered, exaggerated immune response to an antigen that results in tissue damage, disease, or discomfort to the host cell structures.
Down
  1. 1. The structurally diverse class of glycoproteins produced by mature plasma cells that function as antigen-specific antibodies.
  2. 2. A plasma protein mediator produced via the kinin system that causes vascular permeability, smooth muscle contraction, and pain.
  3. 4. Antigens present in some but not all members of the same species, serving as the main targets in organ transplant rejections.
  4. 6. Long-lived mononuclear phagocytic cells that dominate chronic inflammatory sites, orchestrate tissue healing, and present antigens.
  5. 9. The multi-step process where specialized cells engulf, ingest, and destroy foreign particles, microbes, or cellular debris.
  6. 10. The state of immunological unresponsiveness to a particular antigen, essential for preventing the destruction of self-tissues.
  7. 13. Inflammatory lipid mediators derived from arachidonic acid via the cyclooxygenase pathway that directly induce pain and fever.
  8. 16. The primary cellular components of adaptive immunity, divided into antigen-specific T-cell lines and antibody-producing B-cell lines.
  9. 17. A small molecule that is not immunogenic on its own but can elicit an immune response after binding to a larger carrier protein.
  10. 18. The clinical term for redness at an inflammatory site, driven primarily by localized vasodilation and increased microvascular blood flow.
  11. 19. The target enzyme inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs) to disrupt the synthesis of pro-inflammatory eicosanoids.
  12. 20. A vasoactive amine released by mast cells that binds to H1 receptors to cause rapid endothelial cell contraction and edema.
  13. 24. A plasma protein cascade that, when activated, causes opsonization, leukocyte chemotaxis, and membrane attack complex formation.
  14. 25. Deep dermal, subcutaneous, or submucosal swelling caused by vascular permeability shifts, presenting a critical airway hazard.
  15. 27. Any molecule (such as an antibody or C3b fragment) that binds to an antigen to enhance its susceptibility to phagocytic ingestion.
  16. 28. The primary granulocytic phagocytes that arrive first at the site of acute inflammation, dominating the cellular response within 24 hours.