Innate Immunity & Adaptive Immunity Flashcards
Define immune system & infectious disease.
What are the roles of the immune system?
Outline the differences between innate & adaptive immunity.
Immune system= cells and organs that contribute to immune defences against infectious and non infectious conditions (self v non self)
Infectious disease= when the pathogen succeeds in evading and/ or overwhelming the hosts immune defences
-pathogen recognition (cell surface and soluble receptors), containing/ eliminating infection, regulating itself (minimum damage to host), remembering pathogens
-innate; fast w/in secs, lack of specificity,lack of memory, no change in intensity
-adaptive; slow w/in days, specificity, immunologic memory, changes in intensity
The first lines of defence are physical barriers, physiological barriers, chemical barriers & biological barriers. What are they for & outline each
- factors that prevent entry and limit growth of pathogens
- physical=skin, mucous membrane (mouth, resp tract, GI tract, UT), bronchial cilia
- physiological= diarrhoea, vomiting, coughing, sneezing
- chemical barriers= low pH (skin is 5.5, vagina is 4.4), antimicrobial molecules (IgA in tears, saliva etc, lysozymes, mucus, gastric acid8
- biological barriers=normal flora; non pathogenic, strategic positions (nasopharyx, mouth, skin, gi, vagina) *normal flora compete w pathogens for attachment sites and resources, produce anti microbial chemicals and synthesis vitamins like K B12 and other B vits *
Give some examples of normal flora and their respective locations.
- give some ways clinical problems can arise from normal flora
- give examples of patients at higher risk of serious infection
-skin; staphylococcus aureus causes cellulitis, staphylococcus epidermidis, Candida albicans in vagina
-mouth & nasopharynx; streptococcus mutans causes teeth plaque, streptococcus pneumoniae
-GI; E. coli
1- normal flora displaced from its normal location to a sterile location eg breach of skins integrity (skin loss, cuts, burn, IV, surgery), fecal-oral route, fecal-perineal-urethral route (eg women’s UTI), poor dental work
2-normal flora overgrows and becomes pathogenic when host becomes immunocompromised eg diabetes, chemo
3-when normal flora in mucosal surfaces is depleted by antibiotic therapy eg vagina (candida albans will multiply & cause thrush)
-asplenic + hyposlenic, damaged or prosthetic valves
- what are the second lines of defence & what do they do?
- name the 3 main phagocytes and give their functions
- name the other 4 key cells of the IS.
- innate immunity, clear and contain the infection by recognising and killing microbes
- macrophages (in all organs, carry out phagocytosis, is an antigen presenting cell, produces cytokines/chemokines), monocytes (in blood, go to infection site & differentiate at tissues), neutrophils MAIN ONES IN INNATE (in blood, increase during infection, recruited by chemokines, phagocytose bacteria)
- other cells 1)basophils= inflammation, allergic responses 2) eosinophils= defend against worms 3) Natural Killer cells= kill abnormal host cells 4)dendritic cells= present microbial antigens to T cells, initiate adaptive immune system.
- how do phagocytes recognise pathogens?
- what is the name of the coating proteins that help this process? Give examples
- phagocytes have pathogen recognition receptors (PRRs) and pathogens have pathogen associated molecular patterns (PAMPs).
- coating proteins called opsonins carry out opsonisation; bind to microbial surfaces allowing enhanced attachment of phagocytes and clearance of microbes
- eg C3b, antibodies IgG, IgM
After pathogen recognition, it must be engulfed and degraded. What are the two mechanism by which the phagocyte can kill the pathogen ?
- pathogen is engulfed into phagosome, then killed via:
1. Oxygen dependant pathway ie respiratory burst
2. Oxygen independent pathway: lysozyme, proteolytic and hydrolysis enzymes
What is the complement system?
-what are some systemic actions & local inflammatory actions by diff parts of the body in innate immunity?
-composed of multiple serum bacteria
-interact w microbes via diff pathways and essentially guide phagocyte to bacteria
-cytokines/ chemokines carry out chemoattraction
-systemic; liver= opsonins, CRP
-Bone marrow= neutrophil mobilisation
-hypothalamus= increase body temp
Local inflammatory= blood vessels vasodilator, increase vascular permeability
- name the key cells/cell types involved in adaptive immunity
- name and describe the 4 types of antigen presenting cells, state what the cell presents the antigens to.
- give some general features of antigen presenting cells
- naive T cells (never encountered a pathogen before), antigen presenting cells
- 1)dendritic cells=present to naive T cells, aid the T cell response against most pathogens. 2) langerhans cells= present antigens to naive T cells, aid T cell response against most pathogens. 3) macrophages= present to affect or T cells, help w phagocytic activities. 4) B cells= present to effector T cells, help w antibody ie humoral response
- APCs sense, capture, process and present the pathogen. They’re in strategic locations eg skin, mucosal membranes, blood, lymph nodes, they have diverse PRRs and diverse capture methods (phagocytosis-while microbe and macropinocytosis- soluble particles)
- define effector T cells
- describe the process by which a pathogen is presented to a T cell.
- pathogens are presented by MHC molecules on cell membranes of host cells (major histocompatibility complex). What are the 2 classes & give key features of both.
- t cells that have previously encountered the antigen and can do effector functions during an immune response.
- breach of innate barrier, pathogen enters and evade innate mechanisms, APCs (usually macrophages first as they’re in the tissues) will sense, capture, process and express the pathogen, the APCs then travel in the blood stream and lymphatics (MALT- mucosal associated lymphoid tissues, lymph nodes and spleen) to present these antigens to the right T cells
- MHC class I= expressed on all nucleated cells, APCs present intracellular microbes via MHC class I molecules, MHC class II= expressed on all antigen presenting cells APCs, APCs present extra cellular microbes via MHC class II molecules beware for macrophages and some other cells, they’ll be both class I &II as they’re nucleated AND are APCs
- both classes are expressed codominantly, they’re polymorphic genes,
- For viruses and bacteria, would their antigens be presented to MHC I or II molecules?
- describe the processing of intracellular microbes (the endogenous pathway)
- describe the processing of extracellular microbes (the exogenous pathway)
- viruses themselves don’t have a nucleus however they enter into host cells to survive in the body so MHC I molecules are expressed on the host cell AND APCs present intracellular microbes via MHC class I and MHC II is always expressed on APCs
- bacteria=non nucleated, APCs have MHC II expressed on their surface.
- endogenous= viral protein present in cytosol, marked for destruction by proteasome, proteasome generated viral peptide transported to ER by TAP proteins, forms viral peptide-MHC class I complex if right match, occurs in all cell types. APCs and non APCs present the viral peptide to CD8+ molecules on T cells (naive, activated in lymphoid tiss, search for + kill all cells w viral peptide MHC I molecules)
- exogenous=microbes captured by phagocytosis or micropinocytosis, degradation in small peptides in the endosome, peptide rich vesicles fuse w vesicles containing MHC class II molecules, formation of peptide-MHC class II complex if right match, happens only in APCs. (APCs present peptides of extracellular pathogens to CD4+ molecules on T cells)
Define viral tropism.
- give some features of MHC class I and II for peptide presentation
- what are some clinical importances of MHC molecules?
Viral tropism= ability of a given virus to infect a particular cell (cellular tropism), tissue (tissue tropism) or host species (host tropism)
- peptide binding cleft is a variable region w highly polymorphic residues, broadly specific as one MHC can present many peptides, each class has their own responsive T cells (MHC I= CD8+ molecules on T cells *rem class 1x8=8, MHC II= CD4+, class 2x4=8)
- host can deal w a variety of peptides from diff microbes bc of genetic polymorphism, no 2 individuals will have the same set of MHC molecules, ppl will have different susceptibility to diseases, a major cause for transplant rejection, associated w autoimmune disease.
- describe B and T lymphocytes. what is lymphadenopathy.
- what happens when the APCs w antigens on their surface encounter T lymphocytes?
- how are the t lymphocytes then activated?
- what do effector CD4+ T cells and CD8+ T cells become?
- both produced in the BM, T cells need to mature in the thymus, B cells mature after contact w antigen, they are 70% of the cells in blood, accumulate in key lymphoid tissues eg MALT, lymph nodes, spleen
- lymphadenopathy=when t and B cells are activated by the pathogen
- T cells have a T cell receptor on their surface (this recognises the antigens), has a CD3 complex, CD4 or CD8 accessory molecules, very diverse, recognises peptides displayed by MHC molecules (CD4 recognise peptide presented by MHCII molecules, CD8 by MHCI)
- T cells need 2 signals to become activated, the first signal is provided when the T cell receptor binds to the antigen, the second comes when B7 on APCs activates CD28 on T cells. 2 signals is called costimulation.
- CD4= t helper cells, CD8= cytotoxic T cells (CTLs)
- in the activation of the t helper cell response, there are different types of responses. Give the 2 most important and their use.
- how are antigens recognised by B lymphocytes?
- TH1=for cell mediated immunity, differentiation of CD8 T cells, recruits and activates macrophages, B cells produces antibodies:IgG or IgA
- TH2=for humoral immunity, B cells produce IgE, eosinophils kill pathogens, mast cells (allergies)
- CD8 T cells functions=go from naive CD4 cells then via TH1 response they become effector CD8 cells, or naive CD8 cells go and become memory CD8 cells or effector CD8 T cells which become cytotoxic T cells (CTLs) and kill all infected cells (mhcI)
- antigen recognition receptor (called a B cell receptor), unique specificity for each cell, recognises macromolecules and small chemicals
- activation of B lymphocytes requires multiple signals. Describe.
- CD40L, a protein expressed on T cells, is important for Ab production, what’s the only Ab a B cell can make w/o this?
- what is the outcome of b lymphocyte production?
- 1st signal=when the B cell receptor engages w the antigen, signal transduction, 2nd signal=t cell receptor engagement with specific antigen, job of B7. 3rd signal=when the cytokines lead to CD40 activation (a new protein introduced that can switch the type of Ab the B cell produces)
- the only Ab B cell can make w/o CD40L is IgM (therefore needs t helper cells to make other types of Ab)
- after b lymphocytes are activated=Ab production (IgM t helper independent, IgA +IgG +IgE are t helper dependent), memory B cells
- outline the effector functions for the antibodies IgG,IgE,IgA,IgM
- give some medical achievements derived from the study of adaptive immune response.
IgG=fc dependant phagocytosis, inside host, complement activation, neonatal immunity, toxin/virus neutralisation
IgE=immunity against parasites/helmiths, mast cell degranulation (allergies)
IgA=mucosal immunity, mucosal surfaces
IgM=complement activation
-disease prevention via vaccination, immunoglobulin therapies, diagnostic tests
