Infectious Diseases

Innate immune system consists of what stages

• barrier defences

• cellular defences

• inflammatory responses

barrier defence

• physical barriers (epithelial cell layers, secretions)

• chemical barriers (acidic secretions, antimicrobial peptides like lysozyme in tears, defensin)

cellular defences

• phagocytosis (phagocytes have germline-encoded receptors to recognise pathogens)

• induced apoptosis (NK cells release cytotoxic granules to induce cell death of infected cells)

inflammatory response

• phagocytosis by resident tissue macrophages

• release of cytokines and chemokines by macrophages, histamines released by mast cells

• the above cause local vasodilation, increased capillary permeability → accumulation of fluids (swelling)

• chemokines attract leucocytes to site of infection, neutrophiles and macrophages phagocytose to clear debris

• cytokines stimulate fibrinogen to fibrin to clot and seal off injured region

• pyrogens produced to inhibit pathogen reproduction (fever)

antigen presentation

• APCs (eg macrophage, dendritic cells) engulf pathogen, fuse with lysosome to break down, processed antigenic peptide binds to MHC protein to form peptide-MHC complex → activates naive T cells

t cells

• naive TCR binds to peptide-MHC complex on APC cells, undergoes clonal expansion and differentiation to form effector T cells and memory T cells

• helper T cells

  • activates B cells, macrophages and neutrophils

• cytotoxic T cells

  • recognises infected cells, secretes perforins and granzymes to break down cell membrane → death

• memory T cells

b cells

• naive B cells activated by helper T cells, differentiate into plasma cells and memory B cells

• plasma B cells:

  • produces antibodies

• memory B cells

diversity of antibodies

1. somatic recombination → vdj recombination to form different antigen binding sites

2. somatic hypermutation → random mutations that can result in higher affinity Ig chains (affinity maturation)

3. class switching → change in constant segment but same antigen binding site, so different function

function of antibodies

1. neutralisation

2. opsonisation (recognised by phagocytes)

3. ADCC antibody dependent cell-mediated cytotoxicity

types of immunity

active immunity: about antigens

passive immunity: about antibodies (not as effective)

how does antibiotics kill bacteria

• inhibit cell wall synthesis

• inhibit translation

• inhibit nucleic acid synthesis

how is tuberculosis latent

• when tb enters, alveolar macrophages phagocytose bacteria

• in phagosome, bacteria inhibits fusion of lysosome, survives and reproduces

  • even if lysosome fuse, got mycolic acid coat to protect

• some bacteria taken up by dendritic cells present antigen to T cells

• T cells attempt to isolated tb by forming a tubercle around infected macrophages

• at center, cell death by necrosis occurs, rupturing of cell membrane and release of bacteria