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202 Cards in this Set
- Front
- Back
INNATE VS ADAPTIVE IMMUNITY
Receptors? |
Innate: receptors recognizing pathogens are germline encoded
Adaptive: Receptors that recognize pathogen undergo V(D)J recombination during lymphocyte development |
|
INNATE VS ADAPTIVE IMMUNITY
Response time? |
Innate: Fast and Nonspecific, no memory
Adaptive: Slow on first exposure, but memory response is faster and more robust |
|
INNATE VS ADAPTIVE IMMUNITY
What types of cells? |
INNATE
Neutrophils Macrophages Dendritic Cells Natural Killer Cells C' ADAPTIVE T-cells B-cells Circulating Antibody |
|
Locations T-cells progress through during differentiation?
|
Bone marrow
Thymus LN |
|
What stages of T-cells are in the Bone Marrow?
|
Just the T-cell precursor
|
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What stages of T-cells are in the Thymus?
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Cortex: CD4+, CD8+ T cell
Medulla: CD4+ T cell and CD8+ T-cell |
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What happens to the T-cells in the LN?
|
CD8 T's become Cytotoxic T's
CD4 T's become Helper T's (Th1, Th2) |
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Fxn's of Th1 Cells?
|
Make:
IL-2 IFN-gamma Activate: Macrophages CD8 T's Inhibited by: IL-10 |
|
Fxns of Th2 cells?
|
Make:
IL-4 IL-5 IL-10 Help B's make Ab (IgE>IgG) Inhibited by: IFN-gamma |
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What does MHC stand for?
|
Major Histocompatibility Complex
|
|
Who encodes the MCH's?
|
Human Leukocyte Antigen genes (HLA's)
|
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Who specifically encodes MHC I?
|
HLA-A
HLA-B HLA-C |
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Who specifically encodes MHC II?
|
HLA-DR
HLA-DP HLA-DQ |
|
MHC I vs II
location? |
MHC I is on almost all nucleated cells
MHC II is only on Antigen Presenting Cells (APCs) |
|
MHC I vs II
when is the antigen loaded? |
MHC I: loaded in RER of mostly intracellular peptides
MHC II: loaded following release of invariant chain in acidified endosome |
|
What does MHC I do?
|
Mediates Viral Immunity
|
|
Who is MHC I's partner?
|
Beta2-microglobulin
aids in transport to cell surface |
|
Major Fxns of B-Cells?
|
Make Antibody
IgG antibodies opsonize bacteria, neutralize viruses Allergy (Type I hypersensitivity): IgE Cytotoxic (Type II) and Immune Complex (Type III) hypersensitivity: IgG Antibodies cause organ rejection (hyperacute) |
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Major Fxns of T-cells?
|
CD4's help B-cells make antibodies and produce IFN-gamma, which activates Macrophages
Kill virus-infected cells (CD8's) Delayed cell-mediated hypersensitivity (Type IV) Organ rejection (acute and chronic) |
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MOA of Natural Killer Cells?
|
Use Perforin and Granzymes to induce apoptosis of virally infected cells and tumor cells
Only lymphocyte member of innate immune system |
|
What enhances the activity of Natural Killer Cells?
|
IL-12
IFN-beta IFN-alpha |
|
What induces the Natural Killer Cells to kill?
|
Nonspecific activation signal on target cell
and/or Absence of Class I MHC on target cell surface |
|
What binds between T-cells and target cells?
|
CD4 binds to MHC II on APC's
CD8 binds to MHC on virus-infected cells 4 x II = 8 8 x I = 8 |
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What's the CD3 Complex? Fxn?
|
Cluster of polypeptides associated w/ T-cell receptor
Key for signal transduction |
|
Who are the APC's?
|
Macrophages
B-cells Dendritic Cells |
|
How do macrophages and lymphocytes interact?
|
Activated Lymphocytes release IFN-gamma, which activates Macrophages
Macrophages release IL-1 and TNF-alpha which stimulates Lymphocytes |
|
How do Superantigens (toxins) fxn in relation to Lymphocytes/
|
SuperAg's cross-link beta-region of TCR to the MHC II on APC's--> uncoordinated release of IFN-gamma from Th1-cells--->IL-1, IL-6, and TNF-alpha from macrophages
|
|
Who releases superantigens?
|
Strep pyogenes
Staph aureus |
|
How do endotoxins interact w/ lymphocytes?
|
Endotoxins directly stimulate macrophages by binding to endotoxin receptor CD14
Th cells not involved |
|
Who can have endotoxin?
|
gram negatives
|
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How is a Th-cell activated?
|
1. Foreign body phag'd by APC
2. Foreign Ag presented on MHC II and recognized by TCR on Th-cell (signal 1) 3. "Costimulatory signal" given by interaction of B7 and CD28 (signal 2) 4. Th cell activated to produce cytokines |
|
How is a Tc-cell activated?
|
Endogenously synthesized (viral or self) proteins are presented on MHC I and recognized by TCR on Tc-Cell (signal 1)
2. IL-2 from Th-cell activate Tc-cell to kill virus-infected cell (signal 2) |
|
How is B-cell class switching activated?
|
1. IL-4, IL-5, or IL-6 from Th2-cells (signal 1)
2. CD40 receptor activation by binding CD40 ligand on Th-cell (signal 2) |
|
Structure of Antibodies?
|
2 heavy chains
2 light chains Each heavy chain has 3 constant portions and one variable part Each light chain has 1 constant and 1 variable part the Fab portion is composed of the light chains and the half of the heavy chain w/ the variable part The Fc fraction = the other part of the heavy chain (constant) |
|
Fxn of Fab fraction?
|
Antigen-Binding Fragment
Determines Idiotype |
|
Fxn of Fc portion?
|
Constant
Carboxy Terminal C'-binding (IgG and IgM only) Carbohydrate side chains Determines Isotype |
|
3 things an Antibody can do to a bug?
|
Opsonization (promotes phagocytosis)
Neutralization (Ab prevents adherence) C' Activation (enhances opsonization and lysis) |
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How is Antibody diversity generated?
|
1. Random "recombination' of VJ (light chain) or V(D)J (heavy chain) genes
2. Random combination of heavy and light chains 3. Somatic hypermutation (following antigen stimulation) 4. Addition of nucleotides to DNA during "recombination" (see #1) by terminal deoxynucleotidyl transferase |
|
Immunoglobulin Isotypes?
|
IgG
IgA IgM IgD IgE |
|
What do Mature B lymphocytes express on their surfaces?
|
IgM and IgD
|
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What happens when Mature B's undergo Isotype Switching?
|
Alternative splicing of mRNA (mediated by cytokines and CD40 ligand) cause transformation into plasma cells that secrete IgA, IgE, or IgG
|
|
When do we see IgG and what are its Fxns?
|
Main Ab of Secondary response
Most abundant Ig Fixes C' Crosses placenta Opsonizes bacteria Neutralizes bacterial toxins and viruses |
|
When do we see IgA and what are its Fxns?
|
Prevents attachment of bacteria and viruses to mucus membranes
Doesn't fix C' Monomer or dimer Found in Secretions! Picks up secretory component of epithelial cells before secretion? |
|
When do we see IgM and what are its Fxns?
|
Produce in Primary Response to Ag
Fixes C' but can't cross placenta Fxns as Ag receptor on the surface of B-cells Monomer on B-cell or free Pentamer** |
|
Where do we see IgD and what are its Fxns?
|
On surface of many B-cells and in serum
Fxn unclear |
|
Where do we see IgE and what are its fxns?
|
Lowest [ ] in serum
Mediates immediate (type I) hypersensitivity reactions by inducing release of mediators from mast cells and basophils when exposed to allergen. Mediates immunity to worms by activation eosinophils |
|
What the crap is up with Ig Allotypes?
|
Allotypes represent different alleles, so they're the same "species" but are different epitopes
can be on light or heavy chain |
|
What are Ig Idiotypes specific for?
|
a given antigen
|
|
What the heck is a Thymus-Independent Ag?
|
Ag lacking peptide component
Can't be presented by MHC to T cells Stimulate release of IgM antibodies only and can't result in immunologic memory |
|
Examples of Thymus-Indep Ag's?
|
Lipopolysaccharide from cell envelope of Gram-Neg bacteria
Polysaccharide capsular Ag |
|
What are Thymus-dependent Ag's?
|
Antigens containing protein component
Class-switching and immunologic memory occur as a result of direct contact of B's w/ Th's (CD40--CD40 Ligand) and release of IL-4, IL-5, and IL-6 |
|
Important Cytokines?
|
Interleukin 1-6, 8, 10, 12
gamma-Interferon TNF |
|
Where does IL-1 come from and what does it do?
|
Secreted by Macrophages
Causes acute inflammation Induces chemokine production to recruit leukocytes Activates Endothelium to express adhesion molecules An Endogenous Pyrogen (that means fever) |
|
Where does IL-2 come from and what does it do?
|
Secreted by Th Cells
Stimulates growth of helper and cytotoxic T-cells |
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Where does IL-3 come from and what does it do?
|
Secreted by Activated T-cells
Supports growth and differentiation of bone marrow stem cells Fxn similar to GM-CSF(??) |
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Where does IL-4 come from and what does it do?
|
Secreted by activated Th2 cells
Promotes growth of B cells Enhances class switching ---> IgE and IgG |
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Where does IL-5 come from and what does it do?
|
Secreted by Th2 cells
Promotes differentiation of B cells Enhances class switching -->IgA Stimulates production and activation of eosinophils |
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Where does IL-6 come from and what does it do?
|
Secreted by Th cells and Macrophages
Stimulates production of acute-phase reactants and immunoglobulins |
|
Where does IL-8 come from and what does it do?
|
Secreted by macrophages
Major chemotactic factor for neutrophils |
|
Where does IL-10 come from and what does it do?
|
Secreted by regulatory T-cells
Inhibits actions of activated T cells |
|
Where does IL-12 come from and what does it do?
|
Secreted by B cells and macrophages
Activates NK and Th1 cells |
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Where does gamma-interferon come from and what does it do?
|
Secreted by Th1 cells
Stimulates Macrophages |
|
Where does TNF come from and what does it do?
|
Secreted by macrophages
Mediates septic shock Causes leukocyte recruitment, vascular leak |
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Cell Surface Proteins for Helper T Cells?
|
CD4
TCR CD3 CD28 CD40Ligand |
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Cell Surface Proteins for Cytotoxic T Cells?
|
CD8
TCR CD3 |
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Cell Surface Proteins for B Cells?
|
IgM
B7 CD19 CD20 CD21 (receptor for EBV) CD40 MHC II |
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Cell Surface Proteins for Macrophages
|
MHC II
B7 CD40 CD14 Receptors for Fc and C3b |
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Cell Surface Proteins for NK cells?
|
Receptors for MHC I
CD16 (binds Fc of IgG) CD56 |
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Cell Surface Proteins for all cells except mature RBC's?
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MHC I
|
|
What does the Membrane Attack Complex due? When?
|
It defends against gram-negative bacteria
Activated by IgG or IgM in Classic pathway Activated by surface microbes (esp endotoxin) in Alternative pathway |
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Who are the two primary Opsonins in bacterial defense?
|
C3b (aids in clearance of immune complexes too)
IgG |
|
Who is there to help prevent C' activation on self-cells?
|
Decay-Accelerating Factor (DAF)
C1 Esterase Inhibitor |
|
Which C' components are responsible for Viral Neutralization?
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C1
C2 C3 C4 |
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Which C' components can cause anaphylaxis?
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C3a
C5a |
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Which C' component is promotes Neutrophil Chemotaxis?
|
C5a
|
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Which C' components make up the Membrane Attack Complex?
|
C5b
C6 C7 C8 C9 |
|
Alright...what's the classical C' pathway...
|
You start out w/ C1-complex
It gets activated by Ag-Ab complex Activate C1 splits C2 and C4 C4b2a = C3 convertase C3 convertase splits C3 into C3a and C3b C3b joins C4b2a to make C5 convertase |
|
What is the Alternative C' pathway?
|
Starts w/ Spontaneous C3 hydrolysis to form C3a and C3b plus factor B in the presence of factor D gets cleaved into Bb and Ba
Bb binds to C3b --> C3bBb = alt. C3 convertase Alt C3 Convertase cleaves C3 to make more C3b New C3b binds to C3bBb to make C3bBbC3b = alt. C5 convertase |
|
So now that we have C5 convertases, what happens?
|
C5 gets cleaved into C5a and C5b
C5b joins w/ C6, C7, C8, and C9 to form MAC and now the cell is screwed |
|
Where does DAF exhibit its activity?
|
it stops C3 Convertase
|
|
What is the Lectin C' pathway?
|
When Mannose-Binding Lectin binds Mannose, it can cleave C4 and C2
So this pathway skips the C1 complex |
|
What kinds of deficiencies can affect the C' cascade?
|
C1 esterase inhibitor Deficiency
C3 deficiency C5-8 Deficiency DAF Deficiency |
|
What happens as a result of C1 esterase inhibitor deficiency?
|
Hereditary Angioedema
|
|
What happens from C3 deficiency?
|
Severe, recurrent pyogenic sinus and resp. tract infections
Inc susceptibility to Type III hypersensitivity rxns |
|
What does C5-8 def cause?
|
Neisseria bacteremia
|
|
What does DAF Def lead to?
|
C' mediated lysis of RBC's and Paroxysmal Nocturnal Hemoglobinuria
|
|
What do Interferons do to uninfected cells?
|
They place the cells in an antiviral state
|
|
What do Interferons do to viruses?
|
Alpha and Beta Interferons:
Induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA Gamma-Interferons: Inc MHC I and II expression and Inc Ag presentation in all cells They also activate NK cells to kill virus-infected cells |
|
Difference between Active and Passive Immunity?
|
ACTIVE:
Induced after exposure Slow onset Long-lasting protection (memory) PASSIVE: based on receiving preformed Ab's from another host Rapid onset Short life span of Ab's (~3wks) think IgA in boob milk |
|
Classic examples of bacteria who have Ag variation?
|
Salmonella: 2 flagellar variants
Borrelia: relapsing fever N. gonorrhoeae: pilus protein |
|
Classic examples of viruses who have Ag variation?
|
Influenza
major=shift minor=drift |
|
Classic examples of parasites w/ Ag variation?
|
Trypanosomes (programmed rearrangement)
|
|
What is Anergy?
|
Anergy is the failure of a lymphocyte to become activated in response to its Antigen.
Example: Self-reactive T's become nonreactive w/o costimulatory molecule B's can also become anergic, but tolerance is less complete than in T's |
|
Who are the Granulomatous Diseases?
|
TB
Fungal infections (e.g. histo) Syphilis Leprosy Cat Scratch Fever Sarcoidosis Crohn's Disease Berylliosis |
|
How do you get a Giant Cell/
|
You take a Monocyte, it becomes a Macrophage, which becomes an Epitheliod Cell, and finally a Giant Cell
Each transformation is induced by IFN-gamma from Th Cells |
|
Who are some cells of Granulomas?
|
Fibroblasts
Lymphocytes Epitheliod Cells Giant Cells |
|
Types of Hypersensitivity Rxns?
|
Type 1: IgE, Anaphylactic, Atopic
Type 2: Antibody-mediated Type 3: Immune-complex Type 4: Delayed (T-cell mediated) Type |
|
Mechanism for Type 1 Hypersensitivity Rxns?
|
free Ag cross-links w/ IgE on presensitized mast cells and basophils--->release of vasoactive amines that act on postcapillary venules (i.e. histamine)
Rapid Rxn |
|
Tests for Type I Hypersensitivity Rxns?
|
Scratch Test
Radioimmunosorbent Assay |
|
MOA for Type 2 Hypersensitivity Rxns?
|
IgM or IgG bind to fixed Ag on enemy cell--->lysis (C') or phagocytosis
3 MECHANISMS 1. Opsonize cells or attract C' 2. Ab's recruit neutrophils and macrophages that incite tissue damage 3. Bind to normal cellular receptors and interfere w/ functioning |
|
Test for Type 2 Hypersensitivity Rxns?
|
Direct and Indirect Coombs
|
|
MOA for Type 3 Hypersensitivity Rxns?
|
Ag-Ab (IgG) complexes activate C'---> attracts neutrophils--->release lysosomal enzymes
|
|
Test for Type 3 Hypersensitivity Rxns?
|
Immunofluorescent staining
|
|
MOA for Type 4 Hypersensitivity Rxns?
|
Sensitized T lymphocytes encounter Ag and then release lymphokines (leading to mac activation)
|
|
What are the 4 T's of Type 4 Hypersensitivity Rxns?
|
T-Lymphocytes
Transplant Rejection TB skin tests Touching (contact dermatitis) |
|
Test for Type 4 Hypersensitivity Rxns?
|
Patch Test (like PPD)
|
|
Types of diseases cause by Type 1 Hypersensitivity Rxns?
|
Anaphylaxis (bee sting, some food/drug allergies)
Allergic rhinitis (hay fever) |
|
Diseases caused by Type 2 Hypersensitivity Rxns?
|
Hemolytic anemia
Pernicious anemia Idiopathic thrombocytopenic purpura Rheumatic fever Goodpasture's Bullous pemphigoid Pemphigus vulgaris Graves' Myasthenia gravis |
|
Types of Type 3 Hypersensitivity Rxns?
|
SLE
RA Polyarteritis nodosum Poststreptococcal GN Serum Sickness Arthus Rxn Hypersensitivity pneumonia (farmer's lung) |
|
Most common cause of serum sickness?
|
Drugs (not serum)
|
|
Sx's of serum sickness/
|
Fever
Urticaria Arthralgias Proteinuria Lymphadenopathy 5-10 days after exposure |
|
What causes the Arthus Rxn?
|
Intradermal injection of Ag induces Ab's---> complexes in skin
|
|
Sx's of Arthus Rxn/
|
Edema
Necrosis C' activation |
|
What diseases are caused by Type IV Hypersensitivity Rxns?
|
Type 1 Diabetes mellitus
Multiple Sclerosis Guillain-Barre syndrome Hashimoto's Graft-vs-host disease PPD Contact Dermatitis (poison ivy, nickel) |
|
3 of the possible etiologies of SCID?
|
ADA Deficiency
Defective IL-2 receptor MCH II Deficiency |
|
How do you get mature B Cells?
|
Pluripotent Stem Cell
Lymphoid Stem Cell Pro-B cell Pre-B cell Immature B cell IgM, IgG, IgA, IgE producing B's |
|
How do you get mature T cells?
|
Pluripotent Stem Cell
Lymphoid Stem Cell Pro-T Cell Immature T Cell CD8 or CD4 T cell |
|
If you have SCID from an ADA deficiency, where is the problem in the leukocyte dev path?
|
You're stuck at Lymphoid Stem Cells
that's bad |
|
If you have SCID caused by def in IL-2 Receptors, then where is the problem?
|
Can't get from a Pro-T cell to an Immature T-cell
|
|
Where does DiGeorgia interrupt lymphocyte dev?
|
Can't get from an immature T cell to a CD8 or CD4 T-cell
|
|
Where does SCID caused by MHC II def screw up lymphocyte dev?
|
Can't get from a immature T cell to CD4 T's (CD8's ok)
|
|
Where does Selective IgA def screw things up?
|
Between Immature B cell and IgA producing B...all the other isotypes are ok
|
|
Where does Hyper-IgM syndrome screw up lymphocyte development?
|
Stops the pathway from immature B to IgA, IgG, or IgE
so it all goes towards IgM |
|
Where does Common Variable Immunodeficiency screw up lymphocyte dev?
|
It stops the progression from Immature B Cell to anything
|
|
Where does Bruton's Agammaglobulinemia screw lymphocyte dev up?
|
You can't get from Pre-B to Immature B
|
|
4 Broad Categories of Immune Deficiencies?
|
1. Dec Production of...
2. Dec Activation of... 3. Phagocytic cell def 4. Idiopathic dysfunction of... |
|
In what diseases can you have a decreased production of to lead to a Immune Deficiencies?
|
Bruton's Agammaglobulinemia: Dec B Cells
Thymic aplasia (DiGeorge): Dec T Cells SCID w/ Dec B's and T's |
|
What is the most common form of SCID?
|
Defective IL-2 receptors
X-linked |
|
Inheritance of Bruton's?
|
X-Linked Recessive
|
|
Defect in Bruton's?
|
Defective tyrosine kinase gene (BTK)
|
|
Presentation of Bruton's?
|
recurrent bacterial infections starting after 6 months when mom's IgG declines
|
|
Cell #'s in Bruton's?
|
Low levels of all classes of Ig's
Normal Pro-B cell #'s |
|
Pathogenesis of DiGeorge/Thymic Aplasia?
|
Thymus and parathyroids fail to develop b/c failed dev of the 3rd and 4th pharyngeal pouches
|
|
How does DiGeorge present?
|
Recurrent viral and protozoal infections
CATCH-22 Congenital defects of Heart and great vessels. Abnormal facies Thymic aplasia Cleft palate Hypocalcemia-->tetany 22 |
|
Chromosomal defect in DiGeorge?
|
22q11 deletion
|
|
How does SCID present?
|
Recurrent bacterial, viral, fungal, and protzoal infections
No rejection of transplants |
|
What disease causes a decreased activation of T-cells?
|
IL-12 Deficiency
|
|
How does IL-12 Def present?
|
Disseminated mycobacterial infections due to dec Th1 response
|
|
2 diseases leading to dec activation of B cells?
|
Hyper-IgM syndrome
Wiskott-Aldrich Syndrome |
|
Defect in Hyper-IgM-Syndrome?
|
Defect in CD40 Ligand on CD4 T's--->inability to class switch
|
|
How does Hyper-IgM present?
|
Early in life w/ severe pyogenic infections
High IgM and Low IgG, IgA, IgE |
|
Inheritance of Wiskott-Aldrich Syndrome
|
X-linked
|
|
Defect in Wiskott-Aldrich Syndrome?
|
Defect in ability to mount an IgM response to capsular polysaccharides of bacteria
|
|
Levels and Numbers for Wiskott-Aldrich Syndrome?
|
Elevated IgE and IgA
Low IgM |
|
Triad of Sx's for Wiskott-Aldrich Syndrome?
|
Recurrent Pyogenic Infections
Thrombocytopenic purpura Eczema |
|
What disease leads to a decreased activation of Neutrophils?
|
Job's Syndrome
AKA Hyper IgE syndrome |
|
Defect in Job's Syndome?
|
Failure of IFN-gamma production from helper T's, so neutrophils fail to respond to chemotactic stimuli.
|
|
How does Job's present?
|
Coarse Facies
Cold (noninflamed) Staph abscesses Retained Primary Teeth Inc IgE Dermatologic Problems (eczema) |
|
Three different diseases characterized by Phagocytic Cell Deficiency?
|
Leukocyte Adhesion Def Syndrome (type 1)
Chediak-Higashi Syndrome CGD |
|
Defect in Leukocyte Adhesion Def Syndrome (type 1)?
|
defective LFA-1 integrin (CD18) proteins on phagocytes
|
|
How does Leukocyte Adhesion Def Syndrome (type 1) present?
|
Recurrent bacterial infections
Absent Pus Formation Neutrophilia Delayed Separation of Umbilicus |
|
Inheritance of Chediak-Higashi Syndrome?
|
Autosomal Recessive
|
|
Defect in Chediak-Higashi Syndrome?
|
LYST gene
Defective microtubular fxn that screws up lysosomal empyting of phagocytic cells |
|
Presentation of Chediak-Higashi?
|
Recurrent Pyogenic Infections by staph and strep
Partial albinism Peripheral neuropathy |
|
Cause of CGD?
|
Defect in microbicidal activity often from lack of NADPH Oxidase or similar enzymes.
|
|
Presentation of CGD?
|
marked susceptibility to opportunistic infections w/ bacteria (esp Staph aureus and E.coli, and also Aspergillus)
|
|
Dx of CGD w/?
|
Negative Nitroblue Tetrazolium Dye Reduction Test
|
|
What is a disease of Idiopathic dysfunction of T-cells?
|
Chronic Mucocutaneous Cadidiasis
|
|
Defect in Chronic Mucocutaneous Cadidiasis?
|
T Cell dysfxn specifically against candida
|
|
3 diseases w/ idiopathic dysfunction of B-cells?
|
Selective Ig Deficiency
Ataxia-telangiectasia Common Variable Immunodeficiency (CVID) |
|
Most commong Selective Ig Def?
|
IgA def
|
|
Sx's of Selective IgA Def?
|
Sinus and Lung Infections
Milk Allergies and Diarrhea Anaphylaxis upon exposure to blood products containing IgA |
|
Defect in Ataxia-Telangiectasia?
|
Defect in DNA repair enzymes w/ associated IgA def
|
|
Presentation of Ataxia-Telangiectasia?
|
Cerebellar problems
Spider Angiomas (teleangiectasia) |
|
Numbers/Levels for CVID? associated risk?
|
Normal circulating B's
Dec Plasma Cells Dec Ig Inc Risk of autoimmune disease and lymphoma |
|
Autoantibodies and their associated disease
Antinuclear Antibodies (ANA)? |
SLE
|
|
Autoantibodies and their associated disease
Anti-dsDNA and anti-Smith? |
Specific for SLE
|
|
Autoantibodies and their associated disease
antihistone? |
Drug-induced Lupus
|
|
Autoantibodies and their associated disease
Anti-IgG? |
Rheumatoid arthritis
Anti-IgG = Rheumatoid Factor |
|
Autoantibodies and their associated disease
Anticentromere? |
Scleroderma (CREST)
|
|
Autoantibodies and their associated disease
Anti-Scl-70? |
Scleroderma (Diffuse)
|
|
Autoantibodies and their associated disease
Antimitochondrial? |
Primary Biliary Cirrhosis
|
|
Autoantibodies and their associated disease
Antigliadin and Antiendomysial? |
Celiac Disease
|
|
Autoantibodies and their associated disease
Anti-Basement Membrane? |
Goodpasture's
|
|
Autoantibodies and their associated disease
Anti-desmoglein? |
Pemphigus vulgaris
|
|
Autoantibodies and their associated disease
Antimicrosomal and Antithyroglobulin? |
Hashimoto's Thyroiditis
|
|
Autoantibodies and their associated disease
Anti-Jo-1? |
Polmyositis and Dermatomyositis
|
|
Autoantibodies and their associated disease
Anti-SS-A (anti-Ro)? |
Sjorgren's Syndrome
|
|
Autoantibodies and their associated disease
Anti-SS-B (Anti-La) |
Sjorgren's Syndrome
|
|
Autoantibodies and their associated disease
Anti-Ul RNP (Ribonucleoprotein) |
Mixed Connective Tissue Disease
|
|
Autoantibodies and their associated disease
Anti-Smooth Muslce? |
Autoimmune Hepatitis
|
|
Autoantibodies and their associated disease
Anti-Glutamate Decarboxylase? |
Type 1 Diabetes Mellitus
|
|
Autoantibodies and their associated disease
c-ANCA |
Wegener's Granulomatosis
|
|
Autoantibodies and their associated disease
pANCA? |
Other vasculitides
|
|
HLA Subtypes and their associations?
A3? |
Hemochromatosis
|
|
HLA Subtypes and their associations?
B27 |
PAIR
Psoriasis Ankylosing Spondylitis Inflammatory Bowel Disease Reiter's Syndrome |
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HLA Subtypes and their associations?
B8 |
Graves' Disease
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HLA Subtypes and their associations?
DR2 |
Multiple Sclerosis
Hay Fever SLE Goodpasture's |
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HLA Subtypes and their associations?
DR3 |
Type 1 Diabetes Mellitus
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HLA Subtypes and their associations?
DR4 |
Rheumatoid Arthritis
Type 1 Diabetes Mellitus Temporal Arteritis |
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HLA Subtypes and their associations?
DR5 |
Pernicious Anemia--->B12 def
Hashimoto's Thyroiditis |
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HLA Subtypes and their associations?
DR7 |
Steroid-Responsive Nephrotic Syndrome
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What is an Autograft?
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Transplant from self
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What is a Syngeneic Graft?
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Transplant from identical twin or clone
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What is an Allograft?
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Transplant from nonidentical individual of same species
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what is a Xenograft?
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Transplant from a different species
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Who causes a Hyperacute Transplant Rejection?
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Antibody Mediated
Preformed Antidonor antibodies in the recipient Occurs within minutes |
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Who causes an Acute Transplant Rejection?
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Cell-mediated due to Cytotoxic T-Cells reacting against foreign MHC's
Within weeks |
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Rx for Acute Rejection?
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Immunosuppressants such as cyclosporine and OKT3
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Who causes Chronic Transplant Rejection?
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T-cell and antibody mediated vascular damage
Occurs months to years later Irreversible |
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How does Graft-versus-host disease occur?
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Grafted immunocompetent T's proliferate and kick the butt of the irradiated, immunosuppressed host and rejeft the foreign/recipient proteins--->severe organ dysfxn
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Sx's of GvH disease?
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maculopapular rash
jaundice hepatosplenomegaly diarrhea |