MFWB_A - Wild Immunology

natural stressors

climate, demographics (population density, age, sex), resources (nutrition), predictable events (seasonal fluctuations), unpredictable events (emergent disease, injuries, bites)

skin

first line of defence, most effective, fast, non-specific, tissue damage/penetration, trigger danger signals - macrophages, neutrophils, dendritic cells

dendritic cells

if infection isn’t cleared, migrate to lymph nodes and hand antigen to T and B cells, clone expansion, effector T cells migrate to site of infection, trigger antigen-specific B cell expansion

PAMPs gram negative

LPS

PAMPs gram positive

lipoteichoic acid

adaptive response

DCs to lymph nodes via lymphatic vessels, activate naive T cells, diversity and clonal expansion, self-recognising cells deleted

adaptive immunity

(in jawed vertebrates only) somatic recombo of T and B cell receptors by enzymes expressed by recombo-activating genes RAG1 and 2, specialised T and B cells undergo maturation, constant reassortment

wild system constraints

variation - highly variable host of all ages, sexes, nutritional states, history of infection, little prior knowledge, require large sample size (can be difficult if species is rare)

longitudinal sampling

allows before/after, ageing and survival analysis, measurement of reproductive effort, lifetime pathogen transmission quantification, follow individual through time

cross-sectional study

snapshot of population, invasive sampling, parasite burden, fitness readouts, local and systemic tissue extraction, cause and effect not separate

perturbational studies

most powerful as they allow test hypothesis about immune function in wild, medical intervention - chemotherapy (therapeutic) and vaccination (prophylactic), environmental manipulation - dietary supplementation, vector control

why do vaccines fail in wild?

degradation of vaccine immunogenicity