T3 Immunopathology & hypersensitivity Flashcards
main function of cytokines
- chemical signals
- attract cells (chemokines)
main function of acute phase proteins
opsonise pathogens
functions of complement system
- opsonisation
- killing
- activation
- chemoattraction
what do pattern recognition receptors recognise?
- Pathogen-associated Molecular Patterns (PAMPs)
- Danger Associated Molecular Patterns (DAMPs)
examples of pattern recognition receptors
- Toll-like receptors (TLR)
- Inflammasomes (NLRP3)
what are the causative associations of autoimmunity?
- sex:»_space;women
- age:»_space;elderly
- environment: infection; trauma-tissue damage; smoking
how do autoreactive B cells & autoantibodies contribute to autoimmunity?
- directly cytotoxic
- activation of complement
how do autoreactive T cells contribute to autoimmunity?
- directly cytotoxic
- inflammatory cytokines production
typical organ specific autoimmune disease
autoimmune thyroid
typical systemic autoimmune disease
connective tissue diseases
aetiology of Hashimotos thyroditis
- destruction thyroid follicles
- autoimmune
autoantibodies in Hashimotos thyroditis
- thyroglobulin
- thyroid peroxidase
what does Hasimotos thyroditis lead to
hypothyrodism
aetiology of Grave’s disease
- inappropriate stimulation of thyroid gland by anti-TSH-autoantibody
what does Grave’s disease lead to
hyperthyroidism
systemic autoimmune diseases
- systemic lupus erythematosus
- scleroderma
- polymyositis
- sjorgen’s syndrome
- vasculitis
what are the distinctions of an autoinflamamtory disease
- defect in innate immune system
- recurrent inflammation (long term)
- lack of 1ry pathogenic role of adaptive system
what substance is inhibited to treat Muckle-Wells Syndrome
IL-1
what gene is heterozygously mutated in Familial Cold Urticaria, Muckle-Wells Syndrome & NOMID/CINCA (order of severity), on what chromosome
- NLRP3
- Ch1q44
what is the inheritence pattern fo FMU & MWS
AD
symptoms of FCU
- cold induced rash
- arthralgia
- conjuctivitis
symptoms of MWS
- urticarial rash
- sensorineural deafness
- AA Amyloidosis
inheritance pattern of NOMID
sporadic
symptoms of NOMID
- chronic progressive
- meningitis
- destructive arthiritis
table summing up autoimmune vs autoinflammation disease
see weekly summary notes
1ry vs 2ry immunodeficiencies
- 1ry: genetics
- 2ry: external factors
causes of 3ry immunodeficiency
- stress
- surgery
- burns
- malnutrition
- cancer - lymphoproliferative disease
- drugs: affectign lymphocytes & neutrophils
- irradiation
- AIDS
- infections
aetiology of Severe Combined Immunodeficiency (SCID) syndromes
- defect in B&T cells
treatment of SCID
- bone marrow transplantation
- gene therapy
fungi & protozoa causes of defects in T cells
- candida
- pneumocystis
investigations of chemicals in SCID
- normal IgG
- reduced IgM
- no IgA
- reduced/absent T & NK cells
- present B cells
what antibody is involved in type I hypersensitivity reactions and which cells does it degranulate?
- IgE
- mast cells; basophils
what mediators are released in type I hypersensitivity reactions?
- preformed
- de novo synthesized
what are the clinical features of type I hypersensitivity reactions?
- fast onset
- weal & flare
which cells are involved in late phase response in type I hypersensitivity
- eosinophils
- Th2 T cell
what substances are released in 1ry response of type 1 hypersensitivity reactions
- histamine
- proteases
- chemotactic factors
what substances released by 2ry response of type 1 hypersensitivity reactions
- prostoglandins
- leukotrienes
mechanism of type II (cytotoxic) hypersensitivity reaction
IgG/IgM –> complement activation/phagocytosis
clinical features of type II hypersensitivity reactions
- mins - hrs
- lysis & necrosis
common antigens in type ii cytotoxic cells
penicillin
diseases that result in type 2 hypersensitivity reactions
- Goodpasture’s nephritis
- blood transfusion reaction
mode of action in blood transfusion reaction
- complement –> cytotoxic action
- MCA attack complex
mechanism of type 3
- IgG/IgM Ab against soluble antigen - immune complex deposition
- clonal B expansion
clinical features of type 3
- 3-8 hrs
- vasculitis
type 3 associated disease
SLE
mechanism of SLE
- C1 from complement system binds to Ab
- C1-9 +++ increased vessel permeability
- C3&4 in large amount
describe characteristics of vasculitis
- kidneys: complexes in high conc due to filtering
- joint: plasma filtered to synovial fluid
mechanism of type iv hypersensitvity (delayed)
antigen specific T-cell mediated
clinical features of type 4
- 48-72 hrs
- erythema
antigens of type 4
- metals (nickle)
- tuberculin test
- poison ivy
associated disease with type iv
contact dermatitis
summary of hypersensitivity reactions
check out weekly summary
