Immunology - Lecture 26 Flashcards
What are the physical barriers, aka the 1st line of defence?
Skin - largest organ, its own microbe
Gut - lining also epithelial with barrier function
Cillia - hairs lining windpipe move mucus + particles from lung
Urine flow - flushes out pathogens
What are the chemical barriers, aka the 1st lie of defence?
Tears - lysozyme (digest bacteria cell wall)
Mucus, saliva
Openings - secretion of anti-microbrial peptides/enzymes
Stomach acid - HCl secreted by parietal cells = lower pH, this activates proteases (pepsin)
Friendly bacteria - competition
What causes Cystic fibrosis?
Cl- channel mutation causes thick mucus that cilia cannot move
What is an example of a pathogen associated molecular patterns?
LPS in gram negative bacteria cell wall or peptides with formulated methionine (bacteria)
What do damage associated molecular aterns do?
They identify damaged self cells
Innate immunity in macrophages, dendritic cells and neutrophils/
Toll like receptors (TLRs) recognise PAMPs
This do this via a signal cascade via Junlfos TFs and NFRB, causing a change in gene expression
What are myeloid and oymphoid cells invovled in?
Myeloid cell - innate protection
Lymphoid cells - adaptive immunity
WBC (leukocytes) - both myeloid + lymphoid cells
you’re born with it
How do myeloid cells lead to a secondary response?
Myeloid cells (macrophages, dendritic cell) from monocytes + Neutrophils express TLR that recognise pathogenic signal
Cells recognise PAMPs and secrete molecular ligands that attract more immune cells
How can we catch WBCs?
By dilating blood vessels and permeable and sticky endothelial ells
What does swelling of blood vessels cause?
release of inflammatory cytokines (prostoglandins, histomines and cytokines)
What does fever do to immunity?
inhibits proliferation and speed reaction
What is sepsis?
Shock, loss of plasma volume, decreases Blood pressure, causes clotting and a cytokine storm
What phagocytic cells are recruited during the second response?
Neutrophils - short lived(in blood not tissue), migrate to infection sites (puss)
Macrophages - long lived(areas likely to be exposed to pathogens e.. guts, airway)
Eisonophils - attack stuff too large for endocytosis
What is the innate immune repsonse?
Micribes enter through break in skin and phagocytosed by dendritic cell
Activated dendritic cell carries microbial antigens to local lymphnode
What is the adaptive immune response?
Activated dendrtitic cell activates to cells to respond to microbial antigens on dendritic cell surface
How can we link innate and adaptive immunity?
Dendritic cells -> phagocytric cells from monocytes (large variety of TLRs)
Phagocytos pathogen, cleave into peptideswhich are bound to MHC proteins
DCs migrate to lymphoid tissue, activate T-cells of active immune systems
What is adaptive immunity?
Generates specific responses to specifc pathogens
Identifys, target and destroys a vast range of pathogens/toxins
What can be dandgerous about adaptive immunity?
Accidental targeting of self molecules dangerous (GVHD)
How can lymphoid cells generate adaptive immunity?
Lymphoid cells develop in thymus and bone marrow (lymphoid organs). Drains into circulation
They migrate to secondary lymp. organswhere they are exposed to foreign antigens
B cells = bone marrow
T cells = Thymus
WHat are natural killer cells?
Early defence from foreign material and autologous cells under stress e.g. infected (lymphoid cells) or undergoing tumour transformation
What is an antibody reponse?
Secreted solublke immunoglobin binding to antigens.
They are produced by B-lymphocytes and secreted by plasma cells
How many T-cell responses are there?
3 T-cells
What is a Cytoxic T cell?
Directly kills infected host cells
What is a Helper T cell?
Activate macrophages, dendritic cells, B-cells, C-T cells by secreting cytokines and displaying co-stimulatory proteins on surface
What is a Regulatory T-cell?
Inhibits function of T-helper cells, C-T cells and dendrtic cells
What are the steps of Antigen responses?
- In development. library of lymphocytes generated (remain dormant)
- When antigen presented, cells cells complementary are activated
- INcread proliferation and clonal expansion (in vivo selection)
Expansion occurs everytime an antigen is encountered - Triggers differentiation into effector cells
- Subsequent encounter activate memory cells
Boday can respond to many antogens at once
Why is there lag after second encounter ?
Encounter is shorter to make respinse faster and stronger
How much of plasma is made up of antibodies (immunoglobins)?
20%
What are the 2 antogen binding sites?
2 ligt and 2 heavy chains
oWhat are the 5 lasses of immunoglogins?
IgG
IgM
IgA
IgD
IgE
each has its own unique heavy chain and subclasses have their own hinge and tail
How can antigen binidng sites allow antigens to bind?
Each chain has its own constant and variable domain
What are antigen binding doamins made up of?
1 modified Ig domian and 3 hyper variable regions
3D structure of hypervariable domains vary
In vivo evolution to select best structure to interact with antigen
