Term
| b-1 cells are a major type of b cell found in what areas of the body? what type of b cell is a B-1 |
|
Definition
| B-1 major type in peritoneal and pleural cavities. It is the first B cell to develop during FETAL LIFE |
|
|
Term
| What are is the primary type of surface bound immunoglobin on B-1 cells? What is the most common co-receptor on them? |
|
Definition
|
|
Term
| where are marginal zone B cells found primarily |
|
Definition
| in the marginal zone of the Spleen. |
|
|
Term
| what is so unique about thymus independent antigens and their interaction with B or T cells? (TI-1 Ag and TI-2 Ag) Is it direct or indirect. |
|
Definition
| They are antigens from pathogens that have NO DIRECT contact between B cells and TH cells. Instead its done via toll like receptors. |
|
|
Term
| Is there direct contact between B cells annd TH cells in Thymus independent antigens |
|
Definition
|
|
Term
| High doses of TI-1 independent Ag will result in? Low dose results in? |
|
Definition
High dose: polyclonal stimulation (mitogens)
Low Dose: Specific, low affinity, B cell activation. |
|
|
Term
| LPS acts as a TI-1 or TI-2 thymus independent antigen |
|
Definition
|
|
Term
| LPS at low doses acts on what part of the B Cell for it to activate? Results in? |
|
Definition
| Binds to the BCR and TLR4 and results in specific antibodies being released to target LPS |
|
|
Term
| At high doses LPS binds to what part of B cell? What is the result |
|
Definition
| at high doses it nonspecifically triggers cell activation via TLR4 only. Not BCR too. This results in different b cells and more variety of Ab production. |
|
|
Term
| Which type of thymus independent Ag do not require direct TH innervation but do need input from their cytokines |
|
Definition
|
|
Term
| What do TI-2 Ag act on the B cell |
|
Definition
1. Crosslinking to multiple membrane Ig
2. CD21 interaction via Ag-C3D |
|
|
Term
| does TI-1 or TI-2 respond to stimulation by macrophages and dendritic cells? What is the way they communicate |
|
Definition
| TI-2 has BAFF receptors that respond to BAFF expression on dendritic cells and macrophages. |
|
|
Term
| are soluble or insoluble Ag associated with longer lag phases in pirmary response |
|
Definition
| Soluble Ag longer Lag phase than insoluble Ag. So it takes longer for immune response to mount Antibodies for soluble Ag. |
|
|
Term
| peak Ab production for primary response for insoluble and soluble Ag is? |
|
Definition
Peak Ab production for:
1. Soluble: 14 days
2. Insoluble: 7-10 days. |
|
|
Term
| is the decline phase faster in primary or secondary immune response. |
|
Definition
| faster in primary immune response. |
|
|
Term
| affinity maturation occurs primarily in primary or secondary immune response. |
|
Definition
|
|
Term
| In regards to affinity maturation; the degree of affinity or rate of maturation is proportional or inversely proportional to ____ |
|
Definition
| Degree of affinity maturation is INVERSELY proportional to Ag DOSE. |
|
|
Term
| Low concentrations of Ag results in Ab with higher or lower affinity? Whats this refer to? |
|
Definition
| Low Ag concentrations results in higher affinity of Ab. This is referred to as Ab affinity maturation. |
|
|
Term
| what are two ways in which the body or parts in the body contribute to affinity maturation |
|
Definition
1. Concentration levels of Ag inversely decide degrees of affinity
2. somatic hypermutation |
|
|
Term
| what happens in somatic hypermutation |
|
Definition
| contributes to affinity maturation. gene segments for VARIABLE regions of the immunoglobulin chains are altered. |
|
|
Term
| For activation of B cells what needs to happen with signals? Which ones? |
|
Definition
need 3 sequential signals:
Signal 1: B cell BCR binds with Ag
Signal 2: CD40L on TH bind with CD40 on B cells
Signal 3: Cytokines form activated APC or TH |
|
|
Term
| Proliferation of B cells requires what signal? |
|
Definition
| Signal 3: cytokines from either activated APC or TH cells. |
|
|
Term
| differenation of B cells requires what |
|
Definition
| cytokines from actviated APC or TH Cells |
|
|
Term
| name three B cell stimulatory coreceptor complexes |
|
Definition
| 1. CD19 (Intracellular signaling component) 2. CR2 (CD21) 3. TAPA-81 (Target for Anti-proliferative Antigen-1) |
|
|
Term
| Name the B cell inhibitory co-receptor and what it does |
|
Definition
| CD22 = B cell inhibitory co-receptor. Present in a BCR of a resting B cell. Prevents random intracellular signal when there is no Ag. |
|
|
Term
| Ag bindings to BCR results in the complex being engulfed into the B cells to be broken into small fragments. This subsequently is paralleled with increase presentation of what things on B cell as well |
|
Definition
| 1. Increase MHC Class II w/processed Ag 2. B7&B71 (CD80 and CD86) 3. Chemokine receptor CC47 4. increase in CD40 5. placement of IL-2,4,5 receptors 6. ICAM-1 7. ICOS-L |
|
|
Term
| naive T cells need ___ cells to become activated prior to them interacting with activated B cells to cause those B cells to undergo further differentaiotn and proliferation |
|
Definition
| NEed Dendritic cells with Ag- on their MHC II. |
|
|
Term
| can Activated B cells activate TH Naive cells? If so, when would this happen |
|
Definition
| YES can happen if low Ag concentrations and not a lot of dendritic cells floating around presenting them. |
|
|
Term
| In the less common chance that activated B cells present Ag-MHC II to naive T cells would this occur in primary or secondary immune response? Why |
|
Definition
| SEcondary!! Because of memory cells there will be plenty of activated B cells that are easily capable of recognizing Ag and presenting them fast to T cells. BC OF THEIR HYPERMUTATION, Somatic mutation, and so on from primary response. They have higher affinity and therefore require less #'s of B cell presenting antigen |
|
|
Term
| the most potent activating signal for B - T cell interaction is? |
|
Definition
|
|
Term
| CD40L-CD40 signalling does what to the B cells 2x |
|
Definition
1. Stimulates B cell to go from G0 to G1
2. Necessary for Formation of memory b cells |
|
|
Term
| is CD40L expressed on T or B cells. Is it before or after activation |
|
Definition
| On T cells AFTER ACTIVATION BY APC OR Bcells. |
|
|
Term
| What cells release cytokines to influence Activated B cells to isotype switch |
|
Definition
1. TH1
2. TH2
3. macrophages |
|
|
Term
| Do naive TH cells or effector TH cells release cytokines |
|
Definition
| Effector T helper cells like TH1 or TH2 |
|
|
Term
| naive TH cells are primarily activated by ____ in these two areas |
|
Definition
By dendritic cells in
1. lymph nodes
2. spleen |
|
|
Term
| Memory TH Cells can be activated by what three things? Why |
|
Definition
1. macrophages
2. dendritic cells
3. B cells
Can be activated by B cells because memory TH cells have more adhesion molecules as a result of previous primary immune response |
|
|
Term
| activated dendritic cells act as antigen presenting cells. As a result of activation they increase the expression of what three things which will act as the intercommunication with naive T cells |
|
Definition
Dendritic cells increase:
1. MHC I / MHC II +Ag
2. CD80 & CD86
3. cytokines |
|
|
Term
| what is the costimulator on Naive T cells with their TCR/CD4 |
|
Definition
|
|
Term
| signal 2 for TH naive cell is |
|
Definition
|
|
Term
| what is the relationship and action of CD28 and CTLA-4 on T helper cells |
|
Definition
| CD28 acts as a costimulator to the TCR when it communicates with B cells or APCs. AFter enough stimulation the T cells will begin to also place CTLA-4 on surface. Both CTLA 4 and CD28 bind to CD 80 and CD86 of APCs and B cells. CTLA-4 when activated will inihbit further TH activation as a negative feedback system. |
|
|
Term
| signal 3 for naive T cell and APCS/B cell activation is |
|
Definition
|
|
Term
| memory T cells and Effector T cells both add what inducible costimulator |
|
Definition
| ICOS which can bind to ICOS ligands. and make it much easier to activate T cells. |
|
|
Term
| cytokines that influence activation and differentiation of naive T cells are also called ___ cytokines |
|
Definition
|
|
Term
| Polarizing cytokines 3x___ differnetiate or polarize naive T cells into TH-1 cells |
|
Definition
| TH1 cells from: 1. IL12 2. IL18 3. IFN Gamma |
|
|
Term
| Polarizing cytokines 2x___ differnetiate or polarize naive T cells into TH-2 cells |
|
Definition
|
|
Term
| the major IL for T cell activation and proliferation is |
|
Definition
| IL2. The other IL help more with differentiation. (IL4,6 -> TH2 and IL12,18 and IFN --> TH1) |
|
|
Term
| the major IL for T cell activation and proliferation is |
|
Definition
| IL2. The other IL help more with differentiation. (IL4,6 -> TH2 and IL12,18 and IFN --> TH1) |
|
|
Term
| What TH cells secrete IL-3, GM-CSF? (3x) and what does those cytokines do? |
|
Definition
IL-3 and GM-CSF secreted from TH0, TH-1 and TH-2 cells.
1. IL-3: targets production of all blood cells
2. GM-CSF: targets production of granulocytes and macrophages. |
|
|
Term
| What decides whether the immune response will be primarily cell-mediated or Ab response? |
|
Definition
depends on what cytokines are predominate
Ab response favored cytokines :
1. IL-4 - TH2 Cells
2. IL-10 - TH2 cells
Cell mediated immune response favored by:
1. IL12 from APC
2. IL-2 - TH1
3. IFN-gamma - TH1
4. TNF-Beta - TH1 |
|
|
Term
| main target of IL-2 is? Made mostly by which TH cells |
|
Definition
| IL-2 main target is TH1 and it happens to also be made by TH1. (Positive Feed back) |
|
|
Term
| Name three targets of IL-2 |
|
Definition
1. TH1 cells - polife and diffe
2. B cells (minimal)- proliferation
3. Macrophages - activation |
|
|
Term
| B cells are stimulated for IgG2a secretion by what two cytokines |
|
Definition
1. IFN gamma
2. IL 12 from APC |
|
|
Term
|
Definition
1. B cells class switch to IgG2
2. Macrophages / APC
3. Tc cells
4. NK cells |
|
|
Term
| IL-4 released targets? 3x |
|
Definition
1. B cells: early activ and prolif
2. TH2 cells - differnetiation (autocrine)
3. Macrophages - inhibits |
|
|
Term
| what cytokines cause IgE diff |
|
Definition
|
|
Term
| which cytokine targets eosinophils |
|
Definition
|
|
Term
|
Definition
1. target B cells (differen)
2. target TH Cells(prolif and diff - autocrine)
3. target neutrophil
4. Activate T-helper 17 cells
5. ACtivate T-Follicular cells |
|
|
Term
| which T helper cell is associated with chronic inflammation and autoimmunity |
|
Definition
|
|
Term
| what region on TCRs contributes to the excessive non-specific acvitation of T cells by superantigens |
|
Definition
| Variable Beta region on TCRs can be very similar between 5 % of TCRs resulting in polyclonal activation and massive cytokine release |
|
|
Term
| Name the two classes of superantigens |
|
Definition
1. exogenous: soluble proteins,
Example: exotoxins
2. Endogenous: attach to plasma membrane
Example: Viral proteins |
|
|
Term
| Do superantigens cause specific immune response |
|
Definition
| NO. Polyclonal response. LArge activation that is non-specific |
|
|
Term
| Ag-APC interaction occurs where in the body |
|
Definition
|
|
Term
| name the four chemical mediators released from APCs |
|
Definition
1. IL1
2. IL-6
3. TNF-Alpha
4. IL-12 |
|
|
Term
| Direct killing mechanism related to cell mediated immunity include what cells |
|
Definition
1. T cytotoxic cells (CTL)
2. NK Cells
3. Macrophages |
|
|
Term
| Indirect killing mechanisms used by these cell mediated cells are |
|
Definition
| 1. CD4-TH-1 Cells which then stimulate macrophages to do their dirty work |
|
|
Term
| Which type of immune cells can participate in T cell independent responses? |
|
Definition
1. phagocytic cells (eosinophils, macrophages, neutrophils)
2. NK cells |
|
|
Term
| What are the T-cell dependent cell mediated responses |
|
Definition
1. TH1
2. TH2
3. NKT cells
4. T cytotoxic cells |
|
|
Term
| Which T cells release ___ cytokines that reduce TH1 activity |
|
Definition
| TH2 cells secrete IL9, IL10 IL13 that decrease TH1 activity |
|
|
Term
| whats so important about NK cells |
|
Definition
| They can work immediately during discovery of pathogens without the need of Tc cells. |
|
|
Term
| What cytokines can stimulate NK cells |
|
Definition
1. IFN alpha - virus infected cells
2. IFN Beta - virus infected cells
3. IL-12 -from macrophages
4. TNF-alpha - from macrophages |
|
|
Term
| what cytokines sitmulate NK cells to proliferate and secrete IFN gamma |
|
Definition
|
|
Term
| How do NK cells communicate |
|
Definition
| 1. FcR for IgG 2. FasL to bind to Fas on target cell 3. acitvaiton / inhibiton receptors to recognize normal self 4. IFN-Gamma |
|
|
Term
| What do the FasL ligand on NK do? |
|
Definition
| NK Fas ligand sticks into Fas receptor on target cells and causes death via the capase pathway. |
|
|
Term
| can NK cells develop a memory response |
|
Definition
|
|
Term
| Most Effector T cells are this type |
|
Definition
|
|
Term
| What are the five type of targets for T cytotoxic cells |
|
Definition
1. virus infected cells
2. cells infected intracellular by bacteria or fungi
3. tumor cells
4. foreign grafts
5. self cells stressed by temp/trauma |
|
|
Term
| Tc cells require two things for activation |
|
Definition
1. cell-to-cell interaction
2. cytokines |
|
|
Term
| naive Tc cell is also called |
|
Definition
|
|
Term
| Can CTL precursors kill target cells? |
|
Definition
| NO. They are naive Tc cells |
|
|
Term
| apoptosis from Tc cell - target interaction is via two routes |
|
Definition
1. Fas ligand - Fas receptor intereaction causing apoptosis via capase pathway
2. apoptosis via granzme/perforin release from Tc cells and then target cell absorbs them via endocytosis. |
|
|
Term
| How do the granzymes and perforins from Tc cells actually physical work on target cells |
|
Definition
| They are released super close to the target cell after LFA-1 binds to ICAM-1. This marks that the Tc cell and target are close enough for release of their granzymes. Then granzymes and perforin released and stick to target surface. Then they enter the target via receptor mediated endocytosis.That receptor on the surface is mannose-6 phosphate. Perforin is simply there to bore a hole through the vesicle that is formed and let grazymes escape and destroy the cell. Together they act like a trojan horse. |
|
|
Term
| after licensed APC interaction with Tc cell what four things happen |
|
Definition
1. IL-2R increased in TC cell
2. differentiation occurs resulting in granules that contain perforins and granzymes
3. Fas Ligands added to surface
4. IL-2 secreted. |
|
|
Term
| Activation of Tc Cells is usually done where and most often by what cell |
|
Definition
| Done in lyphoid tissues or organs with interaction by LICENSEND APC cells (Dendrites most common) |
|
|
Term
| why is it so much easier to activate memory T c cells? |
|
Definition
| memory Tc cells need less stimuli because they have more adhesion molecules such as CD2 and LFA-1 on their surfaces compared to naive T cells |
|
|
Term
| What complement pathways are iniated by the innate immune system |
|
Definition
1. classical via CRP
2. Alternative
3. Lectin activated |
|
|
Term
| Which complement pathway is activated by the adaptive immune system |
|
Definition
|
|
Term
| the exception to the rule for a and b for small and large complement is |
|
Definition
| C2a is larger and C2b is smaller |
|
|
Term
| What part of the complement is controled by the MHC Class III genes |
|
Definition
Synthesis of:
1. C2
2. C4
3. Factor B
Coding for:
1. C3 |
|
|
Term
| What part of complement is not linked to MHC genes |
|
Definition
|
|
Term
| What antibodies activated the classical complement pathway 4x |
|
Definition
1. IgG1
2. IgG2a
3. IgG3
4. IgM |
|
|
Term
|
Definition
|
|
Term
| Can Complement bind to Fc of Ab if there is not antigen? |
|
Definition
| Complement sites are not open until Ab first is bound to Ag. |
|
|
Term
| name an acute phase protein that can activate the lectin complement pathway |
|
Definition
| MBL - Mannose binding lectin. Binds to mannose on glycoproteins or carbohydrates on surface of pathogens. Then that directly activates complement system. |
|
|
Term
| the most potent chemotaxis complement factor is? Name two other weak ones |
|
Definition
Most potent: C5a
Weak: C3a and C4a |
|
|
Term
| inflammation is comprised of what three properties part of the complement system |
|
Definition
1. chemotaxis: C5a*, C3a, C4a
2. opsonization: C3b*, C4b
3. Anaphylatoxin: C5a*, C3a, C4a
4. Express CAMs for migration: C3a, C5a |
|
|
Term
| What kind of complement can help neutrophils an monocytes express more CAMs |
|
Definition
1. C3a 2. C5a
These have chemotaxis properties so they will increase CAMs on WBCs to get them to migrate to site of invasion . |
|
|
Term
| does soluble or insoluble pathogens get removed via complement+RBCs |
|
Definition
|
|
Term
| what complement factor helps remove pathogesn via opsonization and RBC |
|
Definition
|
|
Term
| Regulators for the complement activation are located where 2x |
|
Definition
1. host cells 2. plasma and tissue fluids
They are located in areas where they will prevent Complement from acting in order to regulate them. Complement acts most on host cells and fre floating in the plasma and other tissue fluids looking for pathogens |
|
|
Term
| What in the plasma inhibits formation or activation of C3 convertase 3x |
|
Definition
| 1. factor H 2. Factor I 3. C4b-binding protein |
|
|
Term
| What regulators to dissociate or inhibit formation of classical or alternative c# convertase are ATTACHED to the plasma membrane |
|
Definition
1. decay accelerating factor (DAF)
2. MEmbrane cofactor protein (MCP) AND CR1 |
|
|
Term
| regulators of complement that attach to the plasma membrane work by inhibiting c3 convertase in what pathways? 2x |
|
Definition
1. classical pathway
- via DAF (CD55) and CR1 (CD35)
2. alternative pathway
- VIA: DAF (CD55) and CR1 (CD35) |
|
|
Term
| can C1q be inactivated? Is it done in the plasma or host cells? |
|
Definition
| yes by C1 inactivator. This is down in the plasma |
|
|
Term
| where is MAC prevented or regulated? By what molecules |
|
Definition
1. plasma by S protein which inactivates free C567 from further development of MAC at
2. plasma membrane by Homologous restriction factor (CD59) (Protectin) AKA MIRL |
|
|
Term
| Which regulator of complement prevents MAC formation by binding to C9 |
|
Definition
| Homologous restriction factor (CD59)(Protectin) |
|
|
Term
| what reuglator inactivates anaphylatoxin and chemotactic activities |
|
Definition
|
|
Term
| in what ways can pathogens screw with complement to keep it from working right 3x |
|
Definition
| 1. can mislead C3b to bind to Factor H (which deactivates it) instead of Factor B 2. Pathogens can have a capsule to prevent interaction between C3b and Complement receptor of a phagocyte 3. Pathogens can develop similar complement components like CR-like, DAF-like, and/or CD59-like molecules to bind to complement and restrict its use. |
|
|
Term
| how many complement receptors are there for C3 |
|
Definition
four
1. CR1 (CD35)
2. CR2 (CD21)
3. CR3 (CD18/CD11b)
4. CR4 (CD18/CD11c) |
|
|
Term
| which of the complement receptors for C3 are on phagocytic cells |
|
Definition
|
|
Term
| All CR receptors except for ___ help with opsonization and phagocytosis |
|
Definition
|
|
Term
| what is affinity maturation |
|
Definition
| In immunology, affinity maturation is the process by which B cells produce antibodies with increased affinity for antigen during the course of an immune response. With repeated exposures to the same antigen, a host will produce antibodies of successively greater affinities. A secondary response can elicit antibodies with several logfold greater affinity than in a primary response. |
|
|
Term
| In a B cell primary response to a thymus‐dependent antigen, the immune system selects B cells with what kind of affinity |
|
Definition
| In a B cell primary response to a thymus‐dependent antigen, the immune system selects B cells with a high affinity and specificity for the antigen and these become memory cells. |
|
|
Term
| The ______ immune system is the first line of defence against infectious agents. When this is breached, the ____ immune system provides a more efficient response to clearing pathogens. |
|
Definition
| The innate immune system is the first line of defence against infectious agents. When this is breached, the adaptive immune system provides a more efficient response to clearing pathogens. |
|
|
Term
| The selection of B cells with a high affinity for a given antigen occurs in |
|
Definition
| The selection of B cells with a high affinity for a given antigen occurs in the germinal centres of secondary lymphoid follicles |
|
|
Term
| The ability to change the isotype of antibody produced (class switching) by a B cell also occurs in |
|
Definition
| The ability to change the isotype of antibody produced (class switching) by a B cell also occurs in germinal centres |
|
|
Term
|
Definition
| Anergy is a term in immunobiology that describes a lack of reaction by the body's defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance. An individual in a state of anergy often indicates that the immune system is unable to mount a normal immune response against a specific antigen, usually a self-antigen. Lymphocytes are said to be anergic when they fail to respond to their specific antigen. Anergy is one of three processes that induce tolerance, modifying the immune system to prevent self-destruction |
|
|
Term
| how many C9's can be added to make variations in the membrane attack complex of complement? |
|
Definition
|
|
Term
|
Definition
| Granzymes are serine proteases that are released by cytoplasmic granules within cytotoxic T cells and natural killer (NK) cells. They induce programmed cell death in the target cell, thus eliminating cells that have become cancerous or are infected with viruses or bacteria |
|
|
Term
| explain how IL2 acts as a autocrine signal for TH1 cells |
|
Definition
| Another example occurs in activated T cell lymphocytes, i.e., when a T cell is induced to mature by binding to a peptide:MHC complex on a professional antigen-presenting cell and by the B7:CD28 costimulatory signal. Upon activation, "low-affinity" IL-2 receptors are replaced by "high-affinity" IL-2 receptors consisting of α, β, and γ chains. The cell then releases IL-2, which binds to its own new IL-2 receptors, causing self-stimulation and ultimately a monoclonal population of T cells. These T cells can then go on to perform effector functions such as macrophage activation, B cell activation, and cell-mediated cytoxicity |
|
|
