Immune System Overview Flashcards
What causes athlete’s foot
Trichophytom rubrum (fungi)
What is the innate immune system
0-96 hours, broad recognition, no memory, macrophages, NK cells and neutrophils
What is the adaptive immuen system
slower, 4-7 days, specific recognition. Memory/recall response. T cells and B cells
What are the roles of the cell in the innate immune system
Phagocytosis - bactericidal killing e.g. respiratory burst
Nitric oxide production and T cell activation
Pathogen recognition - T cell activation
What do CD4 T cells do
produce cytokines to activate macrophages and B cells and to regulate immune response
What do CD8 T cell do
recognise and kill infected cells in a specific manner. Produce cytokines
What are the 5 inflammatory cascades
complement, coagulation, bradykinin, arachidonic acid, free radicals
What does thrombin do
activates coagulation - increases vascular permeability and neutrophil taxis
What does pain activate
Bradykinin pathway - increases vascular permeability, vasodilation, pain, smooth muscle contraction.
What does arachidonic acid pathway activate
Arachidonic acid pathway from tissue damage. Aspirin and other NSAIDs can block this pathway.
What happens in respiratory burst
free radicals. Neutrophils and macrophages which phagocytose and kill microorganisms in vacuoles. Produces high reactive oxygen species.
What is the role of DCs
DCs is a phagocyte but it’s main duty is to pick up foreign antigen and go to a lymph node to activate T cells. Without cytokines, DCs cannot be activated.
What is a mast cell
contain vasoactive protein called histamine. Causes vasodilation and increases permeability in blood vessels. Has inflammatory mediators (preformed in granules), can be released immediately. Low oxygen tension, direct tissue damage. C3a and C5a receptors. Mediated by IgE. Limited range of TLRs.
How does innate immune system recognise foreign antigens
antigen via PAMPs and PRR. Ingests and destroys foreign antigens (phagocytosis). Instructs other cells - cytokines. Initiates and co-ordinates adaptive immune response.
What is IgE important for
Protection of mucosal surfaces
What is T4 hypersensitivity
: T cell mediated. CD4 (delayed type hypersensitivity) and CD8 + CTL (T cell mediated cytolysis). Macrophage activation: cytokine- mediated inflammation. Direct target cell lysis, cytokines inflammation. Contact dermatitis, graft rejection, rheumatoid arthritis, DM, asthma
What is T3 hypersensitivity
immune complex. Immune complexes of circulating Ags and IgM or IgG Abs. Complement and FcR mediated recruitment and activation of leukocytes. Serum sickness, SLE
What occurs in anaphylaxis
1 - generalised itching, urticarial
2 - Swelling away from the sting, incontinence
3 - Difficulty in breathing
4 - Fall in blood pressure, loss of consciousness
What is DerP1
protein that gets inhaled from house dust mite. Causes mast cells in lungs degranulation. Causes allergic asthma.
Describe T cells formation
cells start as stem cells in bone marrow. Migrate to thymus. Thymus is situated above the heart and between the lungs. Unlike PRRs, T cells are encoded of multiple genes and multiple gene segments. Cutting and splicing of these gene segments causes the generation of specificity and diversity.
How is T cell specificity generated
When developing T cell is in the thymus, the beta chain of the T cell receptor is the first to be cut and spliced. 52 variable regions. Multiple joining regions and multiple constant regions.
- D to J rearrangement
- V to DJ rearrangement
- Transcription
- mRNA splicing
What is Goodpasturesg
autoabs to type IV collagen (found in basement membranes and connective tissue) - type II hypersensitivity reaction)
All patients get glomerulonephritis. Only 40% get lung haemorrhage. None get ear problems.
Glomeruli filter plasma where antibodies are have access to BM. Cochlear BM not accessible to autoabs (e.g. of Ag sequestration - immunological ignorance)
In lung, BM separates alveolar epithelium from capillary endothelium so 40% lung disease caused by damage due to smoking
What happens in central tolerance
deleting editing in thymus and bone marrow
What happens in antigen segreation
physical barrier to self-antigen access to lymphoid system in peripheral organs
What happens in peripheral anergy
cellular inactivation by weak signalling without c-stimulus in secondary lymphoid tissue
What happens in cytokine deviation
differentiation of Th2 cells, limiting inflammatory cytokine secretion in secondary lymphoid tissue and sites of inflammation
What happens in clonal exhausation
poptosis post activation in secondary lymphoid tissue and sites of inflammation
What gene makes px prone to RA
HLA-DR4
What type of hypersensitivity is RA
Type II, III, and IV hypersensitivity. Abs and immune complexes and immune cells all cause damage of the joints.
Release of sequestered antigen -> APC with cross-reacting Ag (molecular mimicry) -> Inappropriate MHC expression on non-APCs
How does rabies cause autoimmunity
Rabies virus glycoprotein has an AA sequence similar to insulin. Immune response directed at rabies virus could potentially react with self-insulin receptor.
How does measles virus cause autoimmunity
Measles virus P3 protein has similar AA sequences to myelin basic protein. Immune response has potential to react with CNS mediating MS.
How do T cell become activated
1 is presentation of MHC peptide antigen to T cell receptor. 2 is co-stimulation. Absence of co-stimulation will lead T cell to apoptosis.
Describe T cell differentiation
There are subsets of CD4 T cells : Th1, Th2 and TH17. These subsets produce different cytokines upon encounter with antigen and activate different cell types. APC presents antigen through MHC to undifferentiated Th0 cell under influence of IL-12. This drives differentiate to Th1.
What does IL-4 do
IL-4 drives the development of the cell to Th2 phenotype.
What are Tregs
Natural Tregs are straight from thymus. Inducible Tregs from the periphery.
Generated in thymus and periphery:
Thymus derived CD4 and CD25 Treg: nTreg
Peripherally generated CD4 and CD25 Treg: iTreg
What are the actions of Tregs
Inhibitory cytokines (anti-inflammatory e.g. IL-10 or TGFbeta) Cytolysis: Treg actively kill effector T cells by apoptosis Targeting DCs: inhibition of DC maturation and function.
