Immunology in context Flashcards
Inflammation
Reaction of vascularised living tissue to local injury
Repair
Replacement of injured tissue by: a) regeneration b) fibroblastic or glial scar tissue
Acute inflammation features
Rapid onset, short duration, stereotyped response, rapid resolution.
Vascular changed in acute inflammation
Initial vasoconstriction, then vasodilation and increase in blood flow. Increased permeability causing leaking of fluid to extracellular space.
Oedema
Collection of extracellular fluid within tissues.
Acute Serous inflammation
Acute inflammation when fluid accumulation is a dominant feature of inflammation.
Exudate in acute inflammation
Extravascular fluid with high protein concentration and cellular debris.
Pus
A thick exudate rich in leukocytes (neutrophils) and cell debris.
Margination and mechanisms behind it.
Margination: rolling over and slowing down of neutrophils and molecules due to adherens to epithelial cell membrane
Mechanisms: Weide-palade cells secrete P and E selectin which migrate to the endothelium where they attract neutrophils and cause them to slow down.
Chemotaxis what it is, 1 example of chemokine and 3 examples of chemokine inducing agents (that cause release of chemokine)
The unidirectional migration of cells (neutrophils) towards a chemokine secreted by the inflamed cell.
IL-8 example of chemokine
3 examples:
- Bacterial products
- Complement system components like c5a
- products of lipoxygenase pathway of arachidonic acid metabolism (leukteiene B4)
Diapedesis and Extravasation
interaction between integrin molecules and endotheilial adhesion molecules such as ICAM-1. cause movement of cells across endothelium (diapedisis) and into tissues following chemokine gradient (exravasation)
Characteristics of chronic inflammation
Associated with presence of mononuclear cells (lymphocytes, macrophages, plasma cells)
proliferation of blood vessels and connective tissue
not always the same
long term.
Causes of a chronic inflammation that are not following an acute inflammation
Persistent infection by intracellular organisms
Exposure to non-degradable substance (e.g. coal)
Autoimmune disease.
Chronic granulomatous inflammation and example.
primary immunideficiency disease in which macrophages collect but are unable to kill off the pathogen. Creates a big lump of cells
Example: pulmunary tubercoulosis
Hypersensitivity, what it is and what molecules mediate it (3).
Immune response due to an allergen. Mediated by IgE, mast cells and Th2 response.
Immediate hypersensitivity response
mast cell degranulation and histamine release, causing wheal and flare (raised lesions and surrounding redness)
How to prove autoimmunity? (2 ways)
- Passive transfer of disease by immune effectors (e.g. IGg antibody from mother to child) 2. Patient gets better after immunity supression.
Immunological role of T cells in Type I diabetes
CD8 t cells mediated killing of T cells
CD4 mediated support of CD8 t cells
Failure of Treg to suppress
Di George syndrome
No thymus so no T cells produced (Primary)
SCID (Severe Combined Immune Deficiency)
Pathways producing pre B-cell and T-cell disrupted. (primary) No b or t cells.
Chronic Granulomatous Disease
Inability of macrophages to form reactive oxygen compound to kill ingested bacteria. (Primary)
Hypergammaglobinemia
Inability to differentiate B cell into plasma cell due to mutation of gene coding for CD40 which is present on plasma B cell surface.
PD1 and PDL1 treatment for cancer functioning
Interaction between controlling molecule (Treg) and cells inhibited with PDL1 and PD1 antibodies, letting more immunosurveillance occur.
Outcomes of acute and chronic inflammation
Role of Th2 in allergic response (from T cell to mast cell degranulation)
Common allergic diseases and therapies. Rare therapies
