Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
84 Cards in this Set
- Front
- Back
|
hematopoiesis
|
the formation and development of red and white blood cells, begins in the embryonic yolk sac during the first weeks of development
|
|
|
primary lymphoid organs
|
provide appropriate microenvironments for the development and maturation of lymphocytes
|
|
|
secondary lymphoid organs
|
trap antigen, generally from nearby tissues or vascular spaces and are sites where mature lymphocytes can interact effectively with antigen
|
|
|
What connects the primary and secondary lymphoid organs?
|
blood vessels and lymphatic systems connect these organs, uniting them into a functional whole
|
|
|
leukocytes
|
white blood cells (WBCs)
|
|
|
all blood cells arise from a type of cell called the...
|
hematopoietic stem cell (HSC)
|
|
|
early in hematopoiesis, a multipotent stem cell differentiates along one of two pathways, giving rise to either a .... or.....
|
lymphoid progenitor cell or a myeloid progenitor cell
|
|
|
progenitor cells
|
have lost the capacity for self-renewal and are committed to a particular cell lineage
|
|
|
lymphoid progenitor cells give rise to...
|
B, T, and NK cells
|
|
|
myeloid stem cells give rise to...
|
progenitors of RBCs, neutrophils, eosinophils, basophils, monocytes, mast cells, dendritic cells, and megakaryocytes
|
|
|
What do MHC molecules on the cell surface display?
|
MHC molecules on the cell surface display peptide fragments of antigens.
|
|
|
What do MHC class I molecules present?
|
MHC class I molecules present antigen derived from proteins in the cytosol.
|
|
|
What do MHC class II molecules present?
|
MHC class II molecules present antigen originating in intracellular vesicles.
|
|
|
What is the most important difference between the two classes of MHC molecules?
|
The most important difference between the two classes of MHC molecules is not in their structure but in the source of the peptides that they trap and carry to the cell surface.
|
|
|
TH1 cells recognize...
|
complex of bacterial peptide with MHC class II and activates macrophage
|
|
|
Helper T cell recognizes...
|
complex of antigenic peptide with MHC class II and activates B cell
|
|
|
Cytotoxic CD8 T cells recognize...
|
antigen presented by MHC class I molecules and kill the cell.
|
|
|
MHC class II molecules present antigen originating in...
|
intracellular vessicles
|
|
|
What is the difference between innate immunity and adaptive immunity?
|
Innate immunity serves as a first line of defense but lacks the ability to recognize certain pathogens and to provide the specific protective immunity that prevents reinfection. Adaptive immunity is based on clonal selection from a repertoire of lymphocytes bearing highly diverse antigen-specific receptors that enable the immune system to recognize any foreign antigen.
|
|
|
There are two major types of T cells. What are they and what is the function of each?
|
Cytotoxic CD8 T cells that kill infected target cells, and CD4 T cells that mainly activate macrophages and B cells.
|
|
|
What are the three main consequences of complement activation?
|
1-opsonization of pathogens
2-recruitment of inflammatory and immunocompetent cells 3-the direct killing of pathogens |
|
|
What does the MAC consist of?
|
C5b, C6, C7, C8, and C9
|
|
|
What does C3b bind to?
|
C3b binds to complement receptors on phagocytes.
|
|
|
What do C3a and C5a do?
|
C3a and C5a are peptide mediators of inflammation, phagocyte recruitment
|
|
|
What is the function of C3 convertase?
|
C3 convertase cleaves complement component C3 into C3b and C3a.
|
|
|
At what point do all complement pathways converge?
|
The production of the C3 convertase is the point at which the three pathways converge and the main effector functions of complement are generated.
|
|
|
What does C5b do?
|
C5b triggers the late events in which the terminal components of complement assemble into a membrane-attack complex that can damage the membrane of certain pathogens.
|
|
|
What triggers the classical pathway?
|
The classical pathway is triggered by the binding of C1q to Ab complexed w/ Ag by the direct binding of C1q to the pathogen surface, or by the binding of C1q to C-reactive protein bound to the pathogen.
|
|
|
What triggers the lectin pathway?
|
The lectin pathway is triggered by mannose-binding lectin or the ficolin proteins, normal serum constituents that bind some encapsulated bacteria.
|
|
|
What triggers the alternative pathway?
|
The alternative pathway is triggered directly on pathogen surfaces.
|
|
|
What are the three pathways of complement activation?
|
classical, lectin, alternative
|
|
|
What proteins serve as complement receptors?
|
CR1, CR2, CR3, CR4, C1qR
|
|
|
What are the complement peptide mediators of inflammation?
|
C5a, C3a, C4a
|
|
|
What are the complement membrane-binding proteins and opsonins?
|
C4b, C3b
|
|
|
What are the activating enzymes of the complement system?
|
C1r, C1s, C2a, Bb, D, MASP-2
|
|
|
In the complement system, what binds to mannose on bacteria?
|
MBL-mannose binding lectin
|
|
|
In the complement system, what binds to Ag:Ab complexes and pathogen surfaces?
|
C1q
|
|
|
What is the first protein in the classical pathway of complement activation?
|
C1, which is a complex of C1q, C1r, and C1s.
|
|
|
What is C1q composed of?
|
C1q is composed of six identical subunits with globular heads and long collagen-like tails (a bunch of tulips)
|
|
|
What can the C1q heads of the C1 complex bind to?
|
The heads can bind to the constant regions of immunoglobulin molecules or directly to the pathogen surface, causing a conformational change in C1r, which then cleaves and activates the C1s zymogen.
|
|
|
How is MBioS 440 graded?
|
3 100 point mid-terms (60%)
1 200 point final (40%) |
|
|
What are the proteins of the classical pathway of complement activation?
|
C1, C4, C2, and C3
|
|
|
In the classical pathway, what does the active form of C1q do?
|
C1q binds directly to pathogen surfaces or indirectly to Ab bound to pathogens, thus allowing autoactivation of C1r
|
|
|
In the classical pathway, what does the active form of C1r do?
|
C1r cleaves C1s to active protease
|
|
|
In the classical pathway, what does the active form of C1s do?
|
C1s cleaves C4 and C2
|
|
|
In the classical pathway, what does the active form of C4b do?
|
C4b covalently binds to pathogen and opsonizes it. Binds C2 for cleavage by C1s
|
|
|
In the classical pathway, what does the active form of C4a do?
|
C4a is a peptide mediator of inflammation (weak activity)
|
|
|
In the classical pathway, what does the active form of C2a do?
|
C2a is the active enzyme of classical pathway C3/C5 convertase: cleaves C3 and C5
|
|
|
In the classical pathway, what does the active form of C2b do?
|
C2b is a precursor of vasoactive C2 kinin
|
|
|
In the classical pathway, what does the active form of C3b do?
|
Many molecules of C3b bind to pathogen surface and act as opsonins. Initiates amplification via the alternative pathway. Binds C5 for cleavage by C2b
|
|
|
In the classical pathway, what does the active form of C3a do?
|
C3a is a peptide mediator of inflammation (intermediate activity)
|
|
|
Where is complement activation largely confined to?
|
Complement activation is largely confined to the surface on which it is initiated.
|
|
|
What does hydrolysis of C3 cause?
|
Hydrolysis of C3 causes initiation of the alternative pathway of complement.
|
|
|
What determines the extent of complement activation under different circumstances?
|
Membrane and plasma proteins that regulate the formation and stability of C3 convertases determine the extent of complement activation under different circumstances.
|
|
|
How can the alternative pathway of complement activation amplify the classical or the lectin pathway?
|
The alternative pathway of complement activation can amplify the classical or the lectin pathway by forming an alternative C3 convertase and depositing more C3b molecules on the pathogen.
|
|
|
How does complement activated by the alternative pathway attack pathogens while sparing host cells?
|
Host cells are protected by complement-regulatory proteins.
|
|
|
If C3bBb forms on the surface of host cells, how is it rapidly inactivated by complement-regulatory proteins?
|
Complement regulatory proteins of the host cell: complement receptor 1 (CR1), decay-accelerating factor (DAF), and membrane cofactor of proteolysis (MCP). Host cell surfaces also favor the binding of factor H from plasma. CR1, DAF, and factor H displace Bb from C3b, and CR1, MCP, and factor H catalyze the cleavage of bound C3b by the plasma protease factor I to produce inactive C3b (iC3b).
|
|
|
Why does factor H bind preferentially to C3b bound to vertebrate cells?
|
Factor H binds preferentially to C3b bound to vertebrate cells because it has an affinity for the sialic acid residues present on the cell.
|
|
|
Local inflammatory responses can be induced by small complement fragments, especially...
|
C5a
|
|
|
Assembly of the membrane-attack complex generates...
|
a pore in the lipid bilayer of the membrane
|
|
|
What are chemokines?
|
Chemokines are small chemoattractant proteins that stimulate the migration and activation of cells, especially phagocytic cells and lymphocytes. They have a central role in inflammatory responses.
|
|
|
alternative pathway
|
The alternative pathway of complement activation is triggered by the presence of a pathogen in the absence of specific antibodies and is thus part of the innate immune system. It leads to the production of complement protein C3b and its binding to the surface of the pathogen, after which the pathway is the same as the classical and lectin pathways of complement activation.
|
|
|
primary lymphoid organs
|
sites of lymphocyte development-bone marrow (B cell) and thymus (T cell)
|
|
|
secondary lymphoid organs
|
secondary lymphoid organs are the lymph nodes, spleen, and mucosal-associated lymphoid tissues (MALT), in which immune responses are induced, as opposed to primary, in which lymphocytes develop.
|
|
|
hapten
|
Haptens are small molecules that can bind Ab but cannot themselves elicit an adaptive immune response. Haptens must be chemically linked to protein carriers to elicit Ab and T- cell responses.
|
|
|
Helper CD4 T cells
|
Helper CD4 T cells are CD4 T cells that stimulate or 'help' B cells to make Ab in response to antigenic challenge. Both TH2 and TH1 subsets of effector CD4 T cells can carry out this function.
|
|
|
Hematopoiesis
|
Hematopoiesis is the generation of all the cellular elements of blood, and in humans occurs in the bone marrow. All blood cells originate from pluripotent hematopoietic stem cells in the marrow and subsequently differentiate into the different blood cell types.
|
|
|
Humoral immunity
|
Humoral immunity is immunity due to antibodies and is produced as a result of a humoral immune response. Humoral immunity can be transferred to unimmunized recipients by the transfer of serum containing specific antibody.
|
|
|
Complement is a system of...
|
plasma proteins that is activated by the presence of pathogens.
|
|
|
Complement interacts with...
|
pathogens to mark them for destruction by phagocytes.
|
|
|
The classical pathway is initiated by...
|
activation of the C1 complex.
|
|
|
The lectin pathway is homologous to...
|
the classical pathway.
|
|
|
Complement activation is largely confined to...
|
the surface on which it is initiated.
|
|
|
Hydrolysis of C3 causes...
|
initiation of the alternative pathway of complement.
|
|
|
Membrane and plasma proteins that regulate the formation and stability of C3 convertases determine...
|
the extent of complement activation under different circumstances.
|
|
|
Surface-bound C3 convertase deposits...
|
large numbers of C3b fragments on pathogen surfaces and generates C5 convertase activity.
|
|
|
Ingestion of complement-tagged pathogens by phagocytes is mediated by...
|
receptors for the bound complement proteins.
|
|
|
Some fragments of some complement proteins can initiate...
|
a local inflammatory response.
|
|
|
The terminal complement proteins polymerize to...
|
form pores in membranes that can kill certain pathogens.
|
|
|
Complement control proteins regulate...
|
all three pathways of complement activation and protect the host from its destructive effects.
|
|
|
What is the complement?
|
Complement is a system of plasma proteins that can be activated directly by pathogens or indirectly by pathogen-bound Ab, leading to a cascade of rxns that occurs on the surface of pathogens and generates active components w/ various effector functions.
|
|
|
What is the central event in complement activation?
|
The binding of large numbers of C3b molecules to the pathogen is the central event in complement activation.
|
|
|
What are cytokines?
|
Cytokines are small proteins(~25 kDa) that are released by various cells in the body, usually in response to an activating stimulus, and they induce responses through binding to specific receptors.
|
|
|
What are the two major structural families of cytokines?
|
The hematopoietin family and the TNF family.
|
