Term
| What are two main roles of antibodies? |
|
Definition
| Binding of antigen and inactivation via agglutination |
|
|
Term
| What is the strucure of IgA in the mucosa? everywhere else? |
|
Definition
|
|
Term
|
Definition
| Inhibts microbial adherence, neutralizes viruses, neutralizes catalyzes activity of mcirobial enzymes |
|
|
Term
| What is the role of the secretory component of IgA |
|
Definition
| To coat it, and protect the mucosa from pathogen |
|
|
Term
|
Definition
| epithelim above lymphoid tissue , transport antigens through lumen, where dendritic cells can then act as APC |
|
|
Term
| How do the two parts of IgA dimer connect? |
|
Definition
|
|
Term
| How does secretory IgA work |
|
Definition
| It is hydrophillic and mucophobic, so it prevent the antigen from binding to mucous. Coaitng the virus with IgA makes it compelx and leave the DT. |
|
|
Term
| What is the difference between primary and secondary immune response? |
|
Definition
| First is low response within the adaptive system, few Ig's. Secondary uses memory cells, reproduces a bigger reaction and faster |
|
|
Term
| What are the three broad stages of the adaptive immune response? |
|
Definition
| Anitgen recognition, Clonal distribution, Effector phase |
|
|
Term
| Do TCR undergo hypermutation? |
|
Definition
| No! generate diversity mostly through junctional diversity |
|
|
Term
| what cytokine is specifically activated in superantigen activation? |
|
Definition
|
|
Term
| Do strong bacterial antigen precipitate TH1 or TH2 resposnes? |
|
Definition
| TH1 with help of IL-1,IL-2 |
|
|
Term
| How do type 1 allergic reactions occur? |
|
Definition
| Allergens enter via through epithelium, come into contact with mast cells. First time allergens are presented by APC leading to TH! lymphocyte - IL-4. IgE binds Fc receptors on mast cells and basophils - further exposrure leads to degranulation |
|
|
Term
| What will decide if a Th1/2 cell is created? |
|
Definition
| Based on the pre-existing environment of cytokines. IL_4 will promote TH2 but inhibit TH1, while IL_1 and IFN-g does the opposite |
|
|
Term
| Does TH2 response use inteferon? b cells? |
|
Definition
| No interferon (TH1 only) but yes B cells, causing them to class switch to IgA or IgE |
|
|
Term
| What are two ways we can diagnose allergies? |
|
Definition
| Skin prick test, allergy blood test (RAST measures IgE binding antibodies) |
|
|
Term
| What is the action of typical pharmacotherapy against allergies? |
|
Definition
| Using antagonistic drugs like antihistamines to block action of allergic mediators |
|
|
Term
| How does allergy sensitization work |
|
Definition
| Gradually expose the patient to low levels of allergen so that the mast cell become desensitized and skews IgG antibody production. Become sensitized to high levels of allergies, so that when low levels of allergies arise there will be no reaction |
|
|
Term
| How are monoclonal antibodies use to treat allergies? |
|
Definition
| Bind to free and B cell associated IgE, but don't bind to presensitized basophils or mast cells |
|
|
Term
| What is an example of a thymus independent antigen? |
|
Definition
|
|
Term
| What is the role of L-Selectin? how does that tell us about how developed a lymphocyte is? |
|
Definition
| Used to home to peripheral lymph nodes to encounter anitgens, mostly seen in naive cells that are moving purposelessly |
|
|
Term
| Are bacteria typically phagocytosed or endocytosed? Protein antigens? |
|
Definition
| Bacteria - phagocytosis, protein - endocytosis |
|
|
Term
| What is needed for class switching to occur? |
|
Definition
| T - helper 2 cells. Therefore thymus independant antigens won't class switch |
|
|
Term
| Why do B cells need T cells? |
|
Definition
| Class switching (TH2 cells) and creation of B memory cells |
|
|
Term
| Can thymus independant antigens lead to class swithcing or memory cells? |
|
Definition
|
|
Term
| What are the molecules involved in acute inflammation? |
|
Definition
| PRM's that recognize injury and release cytokines for vasodilation. |
|
|
Term
| What does the altered permeability in vessels during inflammation lead to? |
|
Definition
| Allows for neutrophils to marginate via margination to reach site of injury |
|
|
Term
| What is an important cytokine for chronic and systmeic inflammation? |
|
Definition
|
|
Term
| What are the four steps of WBC margination? |
|
Definition
| 1) Selectin expression, 2) Integrins 3) Diapedesis, 4) chemotaxis |
|
|
Term
| How does histamine help with margination? |
|
Definition
| Promotes expression of p-selectin on endothelial cell surface, causes neutrophil to roll and slow and make bonds |
|
|
Term
| What is the role of integrins? where are they found and what activates them? |
|
Definition
| Found on WBC surface, activated by chemokines, and help the WBC to bind to endothelial surface and also marginate between endothelial cells to pass to site of injury |
|
|
Term
| What's the most important chemokine for attraction in WBC margination? |
|
Definition
|
|
Term
| What is the most often cause of L.A.D? |
|
Definition
| Beta-2 integrin deficiency, adhesion moleule. Neutrophils never make it there, leads to infection without purulence |
|
|
Term
|
Definition
| Fluorescence activated cell sorting, sorts cells into two or more containers. Cells are streamed, broken into individual droplets. |
|
|
Term
Differentiating danger vs. homeostasis is ...
Self vs. non self is? |
|
Definition
|
|
Term
| What is the acute phase response? |
|
Definition
| Rise of certain proteins in response to inflammation - CRP, complement upregulate in response to cytokines and destroy pathogen |
|
|
Term
| Why is it said the innate system doesn't distinguish between self and non self? |
|
Definition
| Although it perfectly discriminates, it never undergo selection for it. Rather, it is created to recognize danger molecules, but doens't recognize the cells that produce them |
|
|
Term
| What are 5 roles of complement? |
|
Definition
| Opsonization (by C3b), MAC, Removal of antigen/antibody complexes, chemotaxis (C5a anaphylatoxin) and to activate B cells |
|
|
Term
| What are two anaphylatoxins in complement system? |
|
Definition
|
|
Term
| What cytokines moves to the hypothalamus and induce fever? |
|
Definition
|
|
Term
| What are three manners of phagocytosis/phagocyte degradation of antigen? |
|
Definition
1)LOW PH OF PHAGOSOME
2) Respiratory burst (NADPH, HOCL, NO)
3) Proteolytic enzymes |
|
|
Term
| What is the purpose of vaccination? |
|
Definition
| Stimulate the immune system by recognizing an agent, destroying it, remember it. |
|
|
Term
| Describe the cellular mechanisms of vaccination from antigen presentation to memory cells? |
|
Definition
| Antigen enters system, destroyed by macrophages and presented to T cells (Act as APC). B cell needs T cell help and cytokines to be acivated. Immune system will produce Th2 cells unless macrophage produces IL-12 for TH1 cells, and TH1 then secrete cytokines to destroy the antigen within them |
|
|
Term
| Name 6 different types of vaccines? Give one example |
|
Definition
Killed - influenza, cholera
Attenuated - yellow fever, measles, mumps, rubella
toxoid- tetanus (inactivated toxic components). subunit - fragment of a microorganism, like hepB (only the surface proteins) and conjugate vaccines (influenza type B - link LPS to proteins) |
|
|
Term
| How do glucocorticoids suppress organ rejection? |
|
Definition
| Suppress immunity as inhibit IL-2, reducing T cell proliferation. Affect B cells by diminshing clonal expansion, strong anti-inflammatory effects. Strong effect on macrophages and stop cytokine release |
|
|
Term
| What drug blocks IL-2 signalling? |
|
Definition
|
|
Term
| What do cytostatics and mycophenalic or penicillin drugs do? |
|
Definition
| They inhibit cell division, affecting T and B cells |
|
|
Term
| How does giving antibodies create an immunosupressive treatment? |
|
Definition
| Polyclonal antibodies inhibit T lymphocytes cause their lyssi, via complement. |
|
|
Term
| What three types of matching are done for drug transplantaitons? |
|
Definition
| Blood matching, tissue matching (MHC) and cross matching (checking for preformed anitbodies to mHC) |
|
|
Term
| Why would someone have pre-formed antibodies before organ transplantation? |
|
Definition
| Previous blood transfusion or organ transplant |
|
|
Term
| What are the risks of immunodeficiency? |
|
Definition
| Leads to increased susceptibility to infections (S.Aureus) |
|
|
Term
| Temporally, what are the three times of rejection? |
|
Definition
| Hyperacute, acute and chronic |
|
|
Term
| What causes a hyperacute rejection? |
|
Definition
| Preformed antibodies due to previous blood transfusion. |
|
|
Term
| What mediates acute rejection? How does it happen |
|
Definition
| T cells, DCs diagnose MHC as foreign, migrate into graft, return back to lymph node, present it. |
|
|
Term
| What are the two ways T cells can be activated/presented during acute rejection? |
|
Definition
| T cell can come into contact wtih T cell of donor, MHC II is incopmtable. Other way is through indirect presentation as host dendritic cells migrate to tissue, present a strange part of MHC II and trigger CD4 cells. |
|
|
Term
| Why are MHC molecules so important in tissue transplantations? |
|
Definition
| Because they are highly variable and highly immunogenic, MHC II elecits a great response |
|
|
Term
| What are three ways you can detect rejection? |
|
Definition
| Infilitrating (host T cells) into graft, tissue anatomy being compromised, and an injury to blood vessels |
|
|
Term
| How can you test for preformed anti-HLA antibodies? |
|
Definition
| Called a cross reaction test - higher number of incompatibilities the lower the survival rate |
|
|
Term
| What is the role of T - regulatory cells? |
|
Definition
| CD4 T cells with high expression of IL-2 receptors. Correct unwanted immune response (like where wrong TH dominates) |
|
|
Term
| What are two types of T regs? |
|
Definition
| Il-10 (inhibits TH1) and TGF-b (inhibits both TH1 and TH2) |
|
|
Term
| What is the role of CTLA-4? |
|
Definition
| high affinity ligand that induces T cell inactivation and apoptosis at end of immune response |
|
|
Term
| how are B cells deactivated? |
|
Definition
| Immune complexes activate antigen receptors as well as Fc receptors on B cells - signal transduction leads to inactivation - no help from TH cells |
|
|
Term
| How do anti-histamines work? |
|
Definition
| H1 receptor antagonists - block receptors and prevent activation |
|
|
Term
| What are the three types of innate defenses? |
|
Definition
| Physical (epithelial cells, hair), chemical (sweat, tears, pH) and cellular (macrophages, NK cells) |
|
|
Term
| Give three examples of physical barriers in innate immune system? |
|
Definition
| epithelial barrier of skin (dies and takes microbes with them), epithelium of intestine (tights junctions). Mucus Barriers - trapping of microbes, mucus thickest in colon |
|
|
Term
| How do tears degrade bacteria? |
|
Definition
| has lysozyme enzyme that destroys pG layer in bacteria |
|
|
Term
| What do paneth cells secrete? |
|
Definition
| Alpha defensins - create pores in bacteria. |
|
|
Term
| How does lactoferrin work? where is it present? |
|
Definition
| Breast milk, works by sequestering iron from microbes |
|
|
Term
|
Definition
| Similar to alpha, secreted by epithelial cells |
|
|
Term
| How do commensal microflora prevent pathogen development? |
|
Definition
| Competitive exclusion, produce compounds that are toxic to other bacteria - exercises immune system |
|
|
Term
How do neutrophils kill cells? Eosinophils?
Role of basophils? |
|
Definition
Neutrophils via defensins and myeloperoxidase
Eosinophils - toxic granules like RNA, DNase
Basophils - histamine = proinflammatory factors |
|
|
Term
|
Definition
| Cellular adhesion molecules, activated by TNF-a and IL-1, are responsible for recruitment of phagocytes to area of injury |
|
|
Term
| Which TLRs recognize bacteria? Viruses? |
|
Definition
| 1,2,4-6 and 9 - bacteria, 3,7 and 8 are viruses |
|
|
Term
| What are PAMPs and DAMPs? |
|
Definition
| PAMPs are damage signals from foreign molecules, DAMPs are damaged self cells |
|
|
Term
| What protein helps with LPS binding and cell activation? |
|
Definition
|
|
Term
| What is the mot potent activator of the complement system? |
|
Definition
|
|
Term
| How do you know it's menigitis and not just redness? |
|
Definition
| Press the glass, spots don't go away |
|
|
Term
| Difference between active and passive vaccination? |
|
Definition
Active - apply antigen and immune system has to respond = long term immunity
Passive - inject antibodies, immune system doesn't do anything |
|
|
Term
| How long does it take until isotype switching occurs? |
|
Definition
|
|
Term
| What are subunit vaccines? |
|
Definition
| Part of a killed vaccine, like using surface antigens in influenza b |
|
|
Term
|
Definition
| Purified proteins alone don't elicit immune response, use ALOH to activate inflammasome and stimulate responsiveness |
|
|
Term
| What kind of hypersensitivity reaction are transplants? |
|
Definition
| Type 2 and type 4 (antibody and cellular mediated) |
|
|
Term
| Explain the mouse model of organ donor and rejection betwen A,B and AxB donor? |
|
Definition
| Isografts lead to acceptance, allograft lead to rejection, but if the recipient is AxB, they have A antigen and therefore accept either an A or B graft |
|
|
Term
| What are the four ways the active immune system of the host is activated in a transplant? |
|
Definition
| Donor MHC and recipient T cells, Donor MHC and donor peptides to host T cells, donor MHC and recipient peptides to T cells, and Donor peptides to recipient T cells by recipient APC |
|
|
Term
| What is the most common form of activating the immune system in organ transplantation? |
|
Definition
| Donor tissues (peptides) are recognized as foreign by host APC and presented to host T cells |
|
|
Term
| What type of rejection (hyperacute, acute or chronic) does immunosuppresive therapy best work on? |
|
Definition
| Acute rejection, mediated mostly by cytokines |
|
|
Term
| What is the main problem of chronic rejection? |
|
Definition
| Vascular disease as blood vessels are targeted and vasculature of graft is destroyed |
|
|
Term
| Is CD4 or CD8 more important in rejection? how do we know? |
|
Definition
| CD4 is, because in studies, if you use an anti-CD4 antibody, the graft lives longer than if you give anti-CD8 or just don't do anything |
|
|
Term
| Why is an acute rejection considered a new immune response? |
|
Definition
| New, not presensitized T cells are reacting to foreign (donor) antigen |
|
|
Term
| What are the three manner of preventing transplant rejection? |
|
Definition
| Tissue typing, non-specific immune supression and specific immune supression |
|
|
Term
| What are three drugs typical of nonspecific immune supression? |
|
Definition
| cyclosporin (IL-2 inhibitor, no TH1) azothioprine (cytostatic, inhibits T cell proliferation), steroids used in autoimmune diseases. |
|
|
Term
| What is a type of specific immune supression? |
|
Definition
| Monoclonal antibodies that inhibit T cell signaling from CD4 cells - leaving behind non activated T cells |
|
|
Term
| What is a type of specific immune supression? |
|
Definition
| Monoclonal antibodies that inhibit T cell signaling from CD4 cells - leaving behind non activated T cells |
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