Factors Influencing Immune responses Flashcards
Pro inflammatory cytokines: what they are and whay they do
IL-1,6 and TNK-a Early, induce acute phase proteins. Temperature and behavioural changes TNF-atriggered by LPS Tissue repair: bone resorption; fibroblast proliferation; collagenase synthesis; leuckocyte adhesion
Chemokines and interferon
Chemokines: directcell traffic and aid chemotaxis
Interferons: transient antiviral state, activate NK cells, upregulate HLA expression
Types of CD4+ T cells
TH1: IgM and IgG. Cytotoxic T cells and for acute viral and bacterial infections
TH2: IgG and IgE, for mucosal immunity. Chronic infections and parasites
TH17: Mucosal immunity and promote inflammatory processes
Treg: down regulate other classes
Primitive versus modern environment (circle diagram, larger for primitive)
_____: In primitive times were prevalent almost no existent in modern times.
____ ___ of ____ _____: Is far ____ in modern times
____ _____ ____: far ____ in modern times.
_____ _____ ____ range (antigens in higher concentrations that were more frequent): was ___ in primitive times and is much larger in ____ times.
Parasites: In primitive times were prevalent almost no existent in modern times.
Diverse varieties of infectious organisms: Is far smaller in modern times
Diverse environmental antigens: far smaller in modern times.
Restricted environmental antigen range (antigens in higher concentrations that were more frequent): was small in primitive times and is much larger in modern times.
Immune responsiveness in primitive versus modern times
Primitive: A TH1 and TH2 bias with more focus on a ____ response e.g Helminth ___ and Treg ,parasites, and ____/protozoal infections (___ and Treg)
In modernisation, less of a ____ effect and more ____ leading to more ____ (___ and TH17) and auto ____ and inflammatory disease (___ and TH17)
Primitive: A TH1 and TH2 bias withmore focuson a regulatory response e.g Helminth TH2 and Treg parasites and mycobacterial/protozoal infections (TH1 and Treg)
In modernisation, less of a regulatory effect and more inflammatory leading to more allergies (TH2 and TH17) and auto immunity and inflammatory disease (TH1 and TH17)
Two types of immunodeficiency
note that immunodefiencies are revealed by the type of recurrent infections
Primary/congenital: genetic defect e.g selective IgA deficiency. Can occur in utero
Secondary or acquired: Infection- HIV, drugs- steroids, cytotoxic drugs, systemic disease (renal failure, malnutrition, burns)
When would you start to see congenital immunodeficiemces?
First few months of life (after 4-6 months) due to maternal IgG levels in utero supplementing immunity
Antigen and antibody considerations with immunity
Antigen: similar to self: poor response; HLA affects peptides presented
Antibodies: How good opsonisation is affects response; further responses: high IgM promotes and high IgG diminishes (due to IgM first line activating B cells, IgG later on so high concs might imply memory already?)
Neuroimune network
Autonomic nervous system, endocrine system and immune system.
ANS affects ES and IS
ES affects IS
IS affects ANS and ES
Pro-inflammatory cytokines and NS (IS to ANS)
Act by:
Increasing body temp; increase slow wave sleep; promote illness behaviour
BY
IL-1 acting on vagus nerve branches
IL-1 secreted by astrocytes and glial cells
IL-1 and neurotransmitter activity
Lymph nodes and the ANS (ANS-IS)
Autonomic, sympathetic nerves to all secondary lymphoid organs. Terminate mainly in paracortical regions (CD4 T cell residence and T cells)
Norepinephrine communicates with T cells
Might be linked to sociability, density related to this
Neuroimmune connections
Draw diagram page 210, too long to explain
Implications of influenza experiment
Elderly people caring for alzheimers patients reacted poorer than those who were not, implying stress of doing this altered the outcome and the immune response
