immune disease 1 (W12) Flashcards
innate lymphocytes features?
fast response
not adaptive - born with them and haven’t changed
innate lymphocytes function?
respond quickly to alert signals from sentinel cells near surfaces, and shape the subsequent adaptive immune response with cytokines
what life history factors can predispose you to different types of immunological tuning
nutrition (eg high salt = more inflammatory)
pollutants
chronic infection
sex hormones
immune ageing
2 types of harmful immune reactions
hypersensitivity (allergy)
autoimmunity (intolerance of self antigens that drives tissue damage)
how do we lose self-tolerance enough to cause disease?
neoantigen - self antigens become modified
molecular mimicry - microbe antigens resemble self
damage exposes hidden antigens (eg histones in dna)
majority of autoimmune diagnoses in men or women?
women (80%)
serum autoantibodies?
just having serum autoantibodies alone doesn’t mean disease. low level autoantibodies common with age, some produced after damage may help clear disease
susceptibility genes for autoimmunity?
risk alleles - MHC alleles, affect peptide binding for antigen presentation
why are most autoimmune diseases more common in women
sex steroids
X-chromosome influence autoimmunity
sex steroids and immune system/inflammation
oestrogen usually pro-inflammatory
progesterone usually anti-inflammatory
testosterone immunosuppression
pregnancy effects on RA and SLE (lupus)
RA flares improve
SLE flares worsen
post-partum effects on RA and SLE (lupus)
SLE and RA flares worsen
menopause effects on RA and SLE (lupus)
SLE flares improve, RA flares worsen
what is converted to oestrogen and why in inflamed tissues
androgen converted to oestrogen.
cytokines increase aromatase which cause this. makes tissue more inflammatory
what inhibits conversion of androgen to oestrogen
TNF (cytokine) inhibitors
atopy?
predisposition to become IgE-sensitised to innocuous environmental Ag (allergen)
unwanted anti-parasite immune response to innocuous antigen?
exposure to antigen in skin/mucosa, ILC2 react, dendritic cells migrate and present antigen in node. naive T cells polarise to TH2 cells that induce B cells to switch to IgE production and mature
IgE-mediated mast cell reactions
mast cells collected IgE. Synthesis of PG, LT, cytokines, chemokines. degranulation (histamine, proteases)
immediate and late effects
immediate effects of IgE-mediated mast cell reactions
skin- itch, oedema, redness
airway- mucosal oedema, bronchospasm
gut- colic, diarrhoea, vomiting
blood- anaphylaxis
late effects of IgE-mediated mast cell reactions? what can these be treated with
more oedema
inflammatory cells
glucocorticoids
symptoms of anaphylaxis
difficulty breathing
vascular shock (low bp, tachycardia)
skin- evolving redness, itch, swelling
mucosal oedema
gut spasm
treatment of anaphylaxis
early i.m. adrenaline (+ oxygen, antihistamine, corticosteroid
non-allergen causes of mast cell degranulation?
radiocontrast medium, opiates, NSAID, anaphylotoxins (C3a, C5a), physical (heat/cold/vibration)
chronic example of igE-mediated allergic diseases?
chronic allergic asthma
