Immunity Flashcards
Difference between innate & adaptive immunity
Innate immune system is first line of defence against pathogens
Adaptive immune system is more specialised
Components of adaptive immunity
T cells which form T helper, T cytotoxic & T regulatory cells
B cells which form memory cells and plasma cells (which then form antibodies)
Components on innate immune system
Blood borne = neutrophils, macrophages, basophils, eosinophils, NK cells
Physical barriers = dermis, mucous membranes, saliva, urine/tears, stomach acid
What is major histocompatibility complex (MHC)
Glycoproteins expressed on cell surface that present peptide chains to other cells
MHC class 1 = expressed on surface of most cells
MHC class 2 = primarily on antigen presenting cells (macrophages, dendritic cells, B cells)
Roles of complement system in innate immunity
Pathogen recognition
Opsonisation
Inflammation
Membrane attack complex (MAC) formation
Clearance of apoptotic cells
Links between innate & acquired immunity
Antigen presentation – innate presents antigens from pathogens to acquired (dendritic cells present them to T cells)
Cytokine signaling – innate immune cells produce cytokines (signaling molecules that activate acquired) when pathogen is recognised - cytokines then activate T & B cells
Memory response – memory response from acquired system is activated when innate immune system activated T & B cells which differentiate into memory cells
What are the pathways of complement system
Classical pathway, alternative pathway, lectin pathway
Describe classical pathway of complement system
Activated by binding of antibodies to surface of pathogens
When antibodies bind to pathogens they change shape & expose binding site for first component of complement system, C1q
Binding triggers cascade of events that lead to production of complement components
(Including C3 & C5 which can opsonise pathogens & induce inflammation)
Describe alternative pathway of complement system
Activated by presence of pathogens/foreign surfaces that don’t have antibodies bound to them
Involved spontaneous hydrolysis of complement protein C3 into C3a & C3b
C3b then binds to surface of pathogens, where it can recruit other complement components (including C5) to induce inflammation & opsonisation
Describe lectin pathway of complement system
Activated by binding of lectins (proteins that can recognise specific sugar molecules on surface of pathogens)
When lectins bind to pathogens, they activate complement components including C3 & C5 (leading to inflammation & opsonisation)
Importance of C3
Opsonisation, inflammation, MAC formation, clearance of apoptotic cells
Canine C3 deficiency
Increased susceptibility to infection
Inherited disorder
Homozygote dogs have no serum C3
Trouble making antibodies against certain pathogens
Increased pyometra, pneumonia, sepsis etc.
Porcine factor H deficiency
Inherited recessive autosomal disease
Factor H stops C3b activation
No serum C3
Die of anaemia & renal failure
Outline membrane attack complex
- Complement system activated by 1 of 3 pathways
- MAC formed by sequential binding of complement proteins in specific order (starts with C5b & then C6, C7, C8 & C9) to form complex that can insert into pathogens membrane
- Once inserted into pathogens membrane, MAC creates pore by polymerising multiple copies of C9
- Pore allows fluid to enter pathogen causing it to burst
- Once pathogen is destroyed, MAC is removed from membrane by action of regulatory proteins
What are Koch’s postulates to identify pathogens
- Suspected pathogen must be present in all cases of disease & absent in healthy animals
- Suspected pathogen must be isolated & grown in pure culture
- Cultured pathogen must be capable of causing disease when introduced into healthy host
- Suspected pathogen must be re-isolated from experimentally infected host & shown to be same as original pathogen
