Immunology & SerologyÂ
Have previously been encountered through natural exposure
Reproduce and evolve more rapidly than the host can eliminate them
Strengthen the hosts immune response
Reproduce and evolve more slowly than the host can eliminate them
Have previously been encountered through vaccination
Pain
Increased vascular permeability and edema
Inactivation of macrophages
Influx of leukocytes
Vasodilation
White pulp
M cells
Lysozyme
Beating cilia
Mucus=secreting goblet cells
Erythrocyte: oxygen transport
Natural killer cell: kills virus-infected cells
Macrophage: phagocytosis and killing of microorganisms
Eosinophil: defense against parasites
Lymphocytes: innate immune response
Neutrophil
Monocyte
Basophil
Eosinophil
All of the above are examples of granulocytes
Eosinophil
Basophil
Monocyte
Neutrophil
Lymphocyte
Monocyte: macrophages
B cell: plasma cell
Myeloid progenitor: neutrophil
Large granular lymphocyte: T cell
Megakaryocyte: platelet
Megakaryocytes do not circulate and reside only in the bone marrow
The hematopoietic stem cell gives rise to white blood cells but a different stem cell is the progenitor of red blood cells
Platelets participate in clotting reactions to prevent blood loss
During human development, hemotopoiesis takes place a different anatomical locations
Hematopoeitic stem cells are self-renewing
Artery to lymph node to efferent lymphatic vessel
Afferent lymphatic vessel to lymph node to efferent lymphatic vessel
Efferent lymphatic vessel to lymph node to afferent lymphatic vessel
Venule to lymph node to efferent lymphatic vessel
Afferent lymphatic vessel to lymph node to artery
Efferent lymphatics
Vein
Artery
High endothelial venule
Afferent lymphatics
Soluble proteins
Made by the spleen
Located in extracellular spaces
Some function as proteases once activated
Activated by a cascade of enzymatic reactions
IC3
C3a
C3b
IC3Bb
C3bBb
Factor B and factor H
Factor H and factor I
Factor B and factor I
Decay-accelerating factor and factor H
Decay-accelerating factor and membrane cofactor protein
C5
C6
C7
C8
C9
C3bBb
C3a
C3b2Bb
IC3b
C5b
Blood clot formation
Enhancement of dissemination of microbes into lymphatics and bloodstream
Decrease in blood loss and fluid into interstitial spaces in tissue
Release of infammatory mediators by platelets
Wound healing
Acts as an opsonin by binding to phosphocholine of pathogens
Synthesized by spleen
Induced by elevated IL-6
A member of the pentraxin family
Triggers the classical pathway of complement activation
C-reactive protein
MyD88
LPS-binding protein
TRIF and TRAM
NFKappaB
Organ failure
High mortality rate
Compromised blood supply to vital organs
Blood vessel constriction
Disseminated intravascular coagulation
Cytokines made by pathogens that decrease body temperature
Pathogen products that decrease body temperature
Pathogen products that increase body temperature
Cytokines made by the host that decrease body temperature
Cytokines made by the host that increase body temperature
Immunoglobin light chain: VJ
T-cell receptor alpha chain: VJ
Immunoglobin heavy chain: VJ
T-cell recepot beta chain:VDJ
None of the above is mismatched
Macrophages
T cells
B cells
Dendritic cells
Epithelium
Peptides ranging between 8 and 25 amino acids in length
Not requiring degradation for recognition
Amino acid sequences not found in host proteins
Primary, and not secondary, structure of protein
Binding to major histocompatibility complex molecules on the surface of antigen-presenting cells
When activated, CD8 T cells in turn activate B cells
CD8 is also known as the CD8 T-cell co-receptor
CD8 binds to MHC molecules at a site distinct from that bound by the T-cell receptor
CD8 cells kill pathogen-infected cells by inducing apoptosis
CD8 T cells are MHC class I-restricted
The pathogen is located in extracellular pathogens
CD8 T cells enable macrophages to kill intracellular pathogens
Pathogen-derived peptides bind MHC Class I molecules in endocytic vesicles found ubiquitously in most cell types
MHC class II molecules are expressed ubiquitoously by most nucleated cells
MHC class I molecules are expressed ubiquitously by most nucleated cells
Light-chain constant regions
Heavy-chain constant regions
Light-chain variable regions
Heavy-chain variable regions
Heavy-chain variable and constant regions
IgM and IgD
IgM
IgD
IgM and IgG
IgG
IgE
IgA
IgD
IgE
IgG
IgM
Somatic recombination
Isotype switching
Somatic hypermutation
Clonal selection
Antigen processing
Complement fixation
Neutralization
Isotype switching
Somatic hypermutation
Somatic recombination
B cell receptors are membrane bound and secreted
B cell receptors consist of a variable region and a constant region
B cell receptors lack specificity and can bind to a number of different antigen
B cell receptors possess specificity and can therefore bind only to unique epitopes
B cell receptors undergo affinity maturation as a consequence of somatic hypermutation
The V regions of light chains only
The V regions of heavy chains only
Paired V regions of a single heavy chain and a single light chain
Paired V regions of two light chains
Paired C regions of two heavy chains
Hypervariable loops; framework regions
Constant domains; variable domains
Heavy chains; light chains
Variable gene segments; joining gene segments
Antigenic determinants; complementarity determing regions
Monoclonal antibody production
Isotype switching
Somatic hypermutation
Opsonization
Somatic recombination
Monoclonal antibody production
Isotype switching
Somatic hypermutation
Opsonization
Somatic recombination
V(D)J recombinase
Terminal deoxynucleotidyl transferase
Exonuclease
DNA polymerase
DNA ligase
IgA
IgD
IgE
IgG
IgM
IgA
IgD
IgE
IgG
IgM
Diversification of the V H sub domain but not the V L domain
Synthesized in proliferating B cells during active immune responses
Somatic hypermutation
Isotype switching
Cytosine conversion to uracil
B cell receptors are membrane bound and secreted
B cell receptors consist of a variable region and a constant region
B cell receptors lack specificity and can bind to a number of different antigens
B cell receptors possess specificity and can therefore bind only to unique epitopes
B cell receptors undergo affinity maturation as a consequence of somatic hypermutation
The V regions of light chains only
The C regions of heavy chains only
Paired V regions of a single heavy chain and a single light chain
Paired V regions of two light chains
Paired C regions of two heavy chains
Monoclonal antibody production
Isotype switching
Somatic hypermutation
Opsonization
Somatic recombination
Somatic recombination of V,D, and J segments is responsible for the diversity of antigen-binding sites
Somatic hypermutation changes the affinity of antigen-binding sites and contribues to further diversification
Class switching enables a change in effector function
The antigen receptor is composed to two identical heavy chains and two identical light chains
Carbohydrate, lipid and protein antigens are recognized and stimulate a response
V alpha and C alpha
V alpha and C beta
C alpha and C beta
V alpha and C beta
V alpha and V beta
Lambda light chain; kappa light chain
Heavy chain; lambda light chain
Kappa light chain; heavy chain
Lambda light chain; heavy chain
Kappa light chain; lambda light chain
CD3 gamma
CD3 delta
CD3 epsilon
Zeta
All of the above
Alpha and beta; CD4
Alpha and beta 2-microglobulin; CD4
Alpha and beta; CD8
Alpha and beta 2-microglobulin; CD8
Alpha and beta; gamma delta T cells
Alpha 1, beta 1
Beta 1, beta 2
Alpha 2, beta 2
Alpha 2, alpha 2
Alpha 1, alpha 2
Plasma membrane -- TAP1/2 --- proteasome -- MHC class I -- endoplasmic reticulum
TAP 1/2 -- proteasome -- MHC class I -- endoplasmic reticulum -- plasma membrane
Proteasome -- TAP 1/2 -- MHC class I -- endoplasmic reticulum -- plasma membrane
Proteasome -- TAP 1/2 -- endoplasmic reticulum -- MHC class I -- plasma membrane
Endoplasmic reticulum -- proteasome -- MHC class I -- TAP 1/2 -- plasma membrane
Protease activity, removal of CLIP from MHC class II, binding of peptide to MHC class II, endocytosis, plasma membrane
Endocytosis, protease activity, removal of CLIP from MHC class II, binding of peptide to MHC class II, plasma membrane
Removal of CLIP from MHC class II, binding of peptide to MHC class II, protease activity, endocytosis, plasma membrane
Binding to peptide to MHC class II, endocytosis, removal of CLIP from MHC class II, protease activity, plasma membrane
Plasma membrane, endocytosis, protease activity, removal of CLIP from MHC class II, binding of peptide to MHC class II.
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