Immunology Flashcards
What are the 2 types of immunity
innate (non-specific)
adaptive (specific)
What are the components of innate immunity
-physical barriers (skin)
-mechanical factors (cough/ cilia)
-secretions (tears/ saliva)
-cellular factors (phagocytic/ NK cells)
What are the 2 types of acquired immunity
Cell mediated- T cells
Humoral -B cells/ antibodies
What is an antigen
Anything that brings about an immune response
and
anything that binds specifically to antibodies/ T-cell antigen recpetors.
What are the actions brought about by antibodies binding to antigens
-lysis of bacteria
-neutralization of toxins
-opsonization (mark antigen for other cells to come and destroy)
-antibody dependent cell mediated cytotoxicity
What cells produce antibodies
B cells that differentiate into plasma cells
Where are antibodies produced
lymph nodes
spleen
bone marrow
What are the 5 different classes of immunoglobulins
IgG
IgA
IgM
IgE
IgD
Which is the heaviest Ig/ has the most antibody binding sites
IgM
Which Ig is the most abundant in the plasma AND can cross the placenta
IgG
Which Ig are characteristic of the
primary immune response
secondary immune response
primary= IgM
secondary= IgG
Which Ig is responsible for protection of mucosal surfaces and how
IgA
production of secretions- tears, saliva, sweat, mucus
present in respiratory and GI tract
What are the functions of IgE
anaphylactic reactions
anti-parasitic
stimulates mast cells, basophils and recruits eosinophils
Which Ig cause complement activation
IgG IgM
Functions of IgD
help in B cell differentiation
acts as a lymphocytic membrane receptor
Functions of IgG
Neutralises toxins
opsonizes bacteria
characteristic of secondary immune response
Functions of IgM
opsonizes and agglutinates bacteria
characteristic of primary immune response
What cells are responsible for cell-mediated immunity
T cells
What are the different types of T-cells
CD4- T helper
CD8- cytotoxic T cells
CD25- activated cytotoxic T cells
What is the function of T-helper cells
present antigens and activates CD8, B cells and macrophages
Once activated what do cytotoxic T cells do?
destroy infected target cells
What is MHC and what is their role in the immune response
Major histrocompatibility complex- are genes that code for glycoproteins on membrane surfaces
they present antigens to T cells
Which MHC class presents endogenous/ viral antigens to signal CD8 T cells
Class 1
Which MHC class presents exogenous antigens to signal CD4 T cells
Class 2
HLA associated diseases :
B27
DR 2
DR 3
DR4
HLA B27= ankylosing spondylitis/ reiters disease
HLA DR2= Good pastures
HLA DR3= Hashimotos, Addisons, Myaesthenia gravis
HLA DR4= T1DM
Where do all lymphoid tissue originate from pleuripotent cells
Bone marrow
WHere do cells that are destined to become T and B cells go?
T cells- Thymus
B cells- stay in bone marrow
What are the primary and secondary lymphoid organs
Primary= Thymus + Bone marrow
Secondary= Lymph nodes, spleen, Mucosa Associated Lymphoid tissue (MALT)
What are the 2 complement pathways
What are the functions of different complements (C3a, C4a, C5a, C3b, C5-9)
What are the types of hypersensitivity reactions
Type 1,2,3,4,5 (ACIDS)
What is Type 1 hypersensitivity and what are the factors involved
Type 1- allergy/ anaphylaxis
IgE antibodies bound to allergens/ antigens cause mast cells/ basophils to release mediators that give the symptoms of allergy
What is Type 2 hypersensitivity and what are the factors involved
Type 2= cytotoxic cell mediated
IgG and IgM involved
Circulating antibodies interact with antigens on cell surfaces to cause cell death
eg: rhesus incompatibility, haemolytic anaemia, ITP, transfusion reactions
What is Type 3 hypersensitivity and what are the factors involved
Type3= Immune complex mediated
IgG and IgM involved
Antibody-antigen form complexes and cause inflammatory reactions where they land and activate COMPLEMENT cascades causing tissue destruction
eg: SLE, RA, serum sickness, post-strep glumerulonephritis
What is Type 4 hypersensitivity and what are the factors involved
Type 4= Delayed hypersensitivity
T-cells involved
Takes 2-3 days to develop
eg: Tuberculin test, allergy tests, dermatitis, tissue/ organ transplant rejection
What is Type 5 hypersensitivity and what are the factors involved
Type 5= Stimulating reactions
Antibodies stimulate the receptors against which they act
eg: myaesthenia gravis/ graves (TSH receptor antibodies cause prolonged secretion of thyroid hormones)
Examples of phagocytic cells
neutrophils, monocytes, macrophages, kuppfer cells
Eg of infective causes of Type 3/ immune complex disease
post-strep glomerulonephritis
Hep B/C
CMV
Malaria
What antibodies/ antigens (A/B) does someone with a blood group O have
AB antibodies (can only receive from O)
No antigens (universal donor)
What antibodies/ antigens (A/B) does someone with a blood group AB have
No Antibodies (universal recipient)
AB antigens
What antibodies/ antigens (A/B) does someone with a blood group A have
Group A:
Antibodies-B
Antigens- A
Group B:
Antibodies-A
Antigens-B
What are Kinins and some of their functions
Kinins are polypepides/ proteins/ enzymes
Vasodilation
increased vascular permeability
attract phagocytes
Which conditions show a high titre of:
-ANCA
-pANCA
-AMA
-anti-SMA + ANA + dsDNA
-anti-EMA + ttG
-anti-CCP
-anti-Scl70
ANCA= vasculitis/ polyangitis/ UC
pANCA= PSC
AMA= PBC
anti-SMA/ ANA/ dsDNA= SLE/ autoimmune hepatitis
anti-EMA/ ttG= coeliacs
anti-CCP= RA
anti-SCL70- systemic scelroderma
What are the effects of Thromboxane
vasoconstriction
increased vascular permeability
aggregation of platelets
Timeframes and management of
hyperacute rejection
acute rejection
Hyper acute= mins-hrs [remove donor organ]
accelerated acute= 2-4 days
acute= 1week- 3months [corticosteroids]
chronic= months-years [ciclosporin/ steroids]
Cause and management of hereditary angio-oedema
Caused due to SERPING1 gene mutation
causes reduced levels/ reduced function of C1 esterase inhibitor
causes increased levels of bradykinin
causes inflammation and increased vascular permeability= oedema
What cells produce leukotrienes and what are the actions of leukotrienes
Mast cells
Leukotrienes cause:
vasoconstriction
bronchoconstriction
MOA of ciclosporin in immunosuppression
What do the following hepatitis antigens/ antibodies indicate
anti-HBs
anti-HBc
anti-HBe
HBsAg
HBcAg
HBeAg
IgG HBcAg
IgM HBcAg
anti-HBs (surface)- immunity due to vaccine/ recovery from prev infection
anti-HBc (core)- prev/ current infection
anti-HBe (envelope)- persistent=chronic infection/ less infective
HBsAg- acute infection
HBcAg- acute infection
HBeAg- highly infective
IgG HBcAg- pev infection (G=gone)
IgM HBcAg- acute infection (M= mantenaint)
What are the mediators in the 2 phases of type 1 hypersensitivity response
Early phase:
-histamine
-prostaglandin D2
-leukotrienes C4, D4
-serotonin
-proteases
late phase:
prostaglandins
leukotrienes
bradykinin
What produces the mediators in the early and plate phases of a type 1 hypersensitivity reaction
early= mast cells
late= mediators are products of metabolism of arachadonic acid
Why should hydrocortisone be given following anaphylaxis
to prevent the late phase of type 1 hypersensitivity rxn
(prevents formation of prostaglandins and leukotrienes)
