Diseases of the Immune System Flashcards
1
Q
TLRs, NOD-like receptors/inflammasome, C-type Lectin Receptors are examples of what?
A
Pattern recognition receptors
2
Q
Activation of TLRs leads to the synthesis and secretion of what?
A
NFkB which => cytokines and adhesion molecules
Interferon regulatory factors (IRFs) => antiviral cytokines
3
Q
What receptors send signals through the inflammasome? What does this action result in?
A
NOD-like receptors
Inflammasome activates caspase-1 => IL-1 into biologically active form (GOF will cause periodic fever syndrome)
4
Q
Where are the C-Type lectin receptors located? What do they detect?
A
PM of macrophages and DCs
Detect Fungal glycan => inflammatory rxn to fungi
5
Q
What complement effectors function to cause inflammation?
A
C5a, C3a
6
Q
What complement effectors function to cause phagocytosis?
A
C3b
7
Q
What tissues serve as the location for lymphocyte stem cell generation and B-cell maturation?
A
Bone Marrow
8
Q
What tissues serve as the location where lymphocytes interact with APCs and antigen in circulating lymph?
A
Lymph nodes
9
Q
What tissues serve as the location where lymphocytes interact with blood-born Ag?
A
Spleen
10
Q
Where are Hassall corpuscles located? What are they composed of?
A
Medulla of thymus
Squamous cell nests
11
Q
The medulla of the thymus is where the maturing T-Cells interact with what?
A
Dendritic APCs with high levels of MHC I and II
12
Q
What part of the peripheral lymphoid organs do the T cells predominate?
A
Paracortex
13
Q
What part of the peripheral lymphoid organs do the B cells predominate?
A
Germinal centers
14
Q
What are the actions of the Helper T Cells (CD4+)
A
Activation of macrophages
Promote proliferation and differentiation of T and B lymphocytes
Inflammation
15
Q
What MHC class is located on all nucleated cells and recognize intracellular Ag? What T cells does it present to?
A
MHC Class I
CD8+
16
Q
Where is MHC Class II typically located? What type of Ag do they recognize? What T Cells does it present to?
A
Antigen presenting cells
Recognize extracellular Ag (bacterial, allergens)
CD4+
17
Q
What is the process by which MHC Class I presents to T cells?
A
- Ag recognizes intracell Ag
- Proteosome processes Ag into peptides
- Transport to ER, load into groove of MHC
- MHC-peptide complex presented to CD8+ (cytotoxic) T cells
18
Q
What is the process by which MHC Class II presents to T cells?
A
- Extracell Ag recognized
- Endolysosomal enzymes process Ag into peptides
- Vesicles form w/ peptide and MHC II
- Complex presented to CD4+ (helper) T cells
19
Q
Which chromosome encodes the HLA molecular structure for a given individual?
A
Chromosome 6
20
Q
What HLA molecules are transcribed from the Class I section of chromosome 6?
A
HLA-A
HLA-B
HLA-C
21
Q
What HLA molecules are transcribed from the Class II section of chromosome 6?
A
HLA-DP
HLA-DQ
HLA-DR
22
Q
What is the T-Cell response during Cell-mediated immunity?
A
After presentation of the Ag, T cells go through:
Proliferation
Differentiation
Migration
Killing
23
Q
Which Ab is the first to produced and the biggest?
A
IgM (pentamer)
24
Q
Which Ab has the longest half-life?
A
IgG
(important in fetal protection)
25
What happens to the fetus if mom has an infection involving IgM late in her pregnancy?
Mom will be able to protect herself but fetus will have no protection because IgM is not passed to newborn
26
What Ab is involved in mucosal defense and present in high levels in the colostrum?
IgA
27
What Ab has the shortest half life? What receptor does it bind to on mast cells, basophils, and eosinophils?
IgE
High affinity binding to FC receptors
28
What immune response are NK cells involved in? How are they inhibited?
Innate immunity
Inhibited w/ MHC Class I expression and self MHC molecules
29
What receptor on NK cells recognize damaged cells and activate the NK cells?
NKG2D receptors
30
In a Type I Hypersensitivity rxn, what Ab do B cells switch to? What receptor does this Ab bind to?
IgE
IgE binds onto FcɛRI receptor
31
What interleukins are involved in a Type I Hypersensitivity reaction? What are their functions?
IL-4 - Class switching
IL-5 - Eosinophil activation
IL-13 - Enhanced IgE production
32
What mast cell mediators are involved in the immediate hypersensitivity reaction?
Degranulation - Histamine
Lipid mediators: Leukotrienes B4, C4, D4; Prostaglandin D2; Platelet Activating Factor
Involved in vasodilation, vascular leakage, smooth muscle spasm
33
What mediators are involved in the late phase hypersensitivity reaction? What are their functions?
Cytokines/chemokines - Leukocyte recruitment
34
Allergies and allergic reactions such as hives, angioedema, and anaphylaxis are all examples of what kind of hypersensitivity reaction?
Type I hypersensitivity
35
What leukocytes are recruited in the late phase of the Type I hypersensitivity reaction?
Inflammatory cells: eosinophils, basophils, neutrophils
36
An H&E stain shows a slide of epithelial cells with a dense infiltrate of inflammatory cells with red cells inside. The pt it was taken from has recurrent dysphagia and subsequent weight loss which has been ongoing since childhood. What is this disease?
Eosinophilic esophagitis
(Food Ag-driven disease of childhood, can't swallow effectively/hurts to swallow)
37
What constitutes a Type II hypersensitivity rxn?
Reactions where Ab directly react with Ag present on the cell surface or ECM
Caused by AutoAb or exogenous Ag bound to cell surfaces
38
What Type II Hypersensitivity diseases are caused by opsonization and phagocytosis? What Ag is targeted?
Autoimmune hemolytic anemia - target red cell membrane ptns (Rh blood group Ag, I Ag)
Autoimmune thrombocytopenic purpura - target platelet membrane ptns
39
What is the basic mechanism of Type II Hypersensitivity via opsonization and phagocytosis?
Opsonized cell is recognized by the Fc receptor on the phagocyte and is devoured and lysed
Cell is gone =\> anemia, thrombocytopenia
40
What is the basic mechanism of the Type II Hypersensitivity reaction via Complement and Fc receptor-mediated inflammation?
Fc receptor recognizes and binds to Ag in basement membrane and deposit Ab
Complement is activated =\> Neutrophil enzymes, ROS released into tissues =\> inflammation and tissue injury
41
What Type II Hypersensitivity reactions are caused by complement and Fc receptor-mediated inflammation? What are their target Ag?
Vasculitis caused by ANCA - target neutrophil granule ptns
Goodpasture syndrome - target noncollagenous ptn in basement membrane of kidney glomeruli and lung alveoli
Acute rheumatic fever - streptococcal cell wall Ag, Ab cross-reacts with myocardial Ag
42
What is the basic mechanism of Type II Hypersensitivity reactions via Ab-mediated cellular dysfunction?
Ab inhibits binding of NT or hormone to receptor
Disrupts endocrine and neural signaling
43
What Type II Hypersensitivity reactions are caused by Ab-mediated cellular dysfunction? What are their targets?
Myasthenia Gravis - Target ACh receptor, inhibit ACh binding
Graves disease - Target and stimulate TSH receptor
Insulin-resistant diabetes - target Insulin Receptor, inhibit insulin binding
44
What is the basic mechanism of Type III Hypersensitivity reactions?
1. Ab combines w/ excess soluble Ag, forming large complexes
2. Circulating immune complexes become lodged in BM of epithelia (kidney, lungs, joints, skin)
3. Fragments of complement cause histamine and other mediator release
4. Neutrophils migrate to site of immune complex deposition =\> release enzymes =\> tissue and organ damage
45
What type of hypersensitivity are the arthus reaction and serum sickness? What are the target Ag?
Type III Hypersensitivity
Serum sickness (acute) - Non-human ptn Ag such as diphtheria antitoxin
Serum sickness (chronic) - self Ag
Arthus rxn (local) - rare local effect of vaccination
46
If immunofluorescence is performed on biopsies, how would you differentiate between hypersensitivity reactions?
Pattern of Ab deposition:
Type II: Smooth, linear
Type III: Grainy, granular
47
Where do post-streptococcal cross-reactive Ab act in a Type II reaction? In a Type III reaction?
Type II - act directly on myocardium
Type III - Form immune complexes that deposit in the glomeruli
48
What is the hallmark of a Type IV Hypersensitivity reaction?
Immune granulomas: caused by a variety of agents that induce persistent T cell-mediated immune responses
49
Rheumatoid arthritis, multiple sclerosis, IBS, Type I DM, Psoriasis, and contact sensitivity are all examples of what type of hypersensitivity?
Type IV Hypersensitivity
50
In general, what cytokines mediate Type IV Hypersensitivity reactions?
Th1 and TH17
(except Type I DM - destruction by CTLs, Psoriasis - mainly TH17)
51
If T Cell receptors react with Self-Ag in the thymus, what happens to them?
Apoptosis
52
If T Cell receptors react with Self-Ag in the bone marrow, what happens to them?
They either edit their receptor and continue or undergo apoptosis
(Bend the knee or die)
53
What T cell receptors promote anergy?
CTLA and PD-1
(Help T cells downregulate when self-Ag present, utilized by viruses and tumors =\> blocking CTLA and PD-1 binding can intensify immune response against CA cells)
54
What are Treg cells induced by? What CD do they recognize? What genes do they express?
Induced by TGF-B
Positive for CD4
Express CD25 and FoxP3
55
What is inhibited when Treg cells are suppressed?
Release of IL-10 and TGF-β
Expression of CTLA-4
(supresses maternal response to allow foreign fetus to grow)
56
What is the purpose of AIRE gene? Where does it exert its normal function?
Stimulate expression of proteins that are not normally expressed in the thymus, critical for central tolerance (deletion of immature T cells specific for these Ag)
Exerts function in the thymus
57
What normal process would fail in the absence of normal AIRE? Resulting in what disease process?
Central tolerance
Failure/Mutations in AIRE gene =\> autoimmune polyendocrinopathy
58
What does IPEX stand for?
I - Immune dysregulation
P - Polyendocrinopathy
E - Enteropathy
X - X-linked
59
What mutation is involved in IPEX disease?
FOXP3
60
What normal process fails in IPEX disease?
Development and maintenance of functional CD4 helper T cells
61
What are the 3 criteria for defining pathological autoimmunity?
1. Immune reaction directed against a self-Ag
2. Immune rxn primarily responsible for a pathologic condition
3. No other pathophysiology possible
62
Upon imaging, a pt with back pain shows inflammation in the joints and fusion of the vertebrae. What disease process is this?
Ankylosing spondylitis
63
What gene is ankylosing spondylitis strongly associated with?
Class I HLA allele B27
64
Ankylosing spondylitis generally affects what population?
Young males with family hx of inflammatory joint conditions
65
Polymorphisms in what gene will ultimately lead to Crohn's disease? What process is rendered defective?
NOD-2 =\> defective NOD-like receptor =\> ineffective innate immune response
Paneth cells become ineffective at microbe killing =\> accumulation of bacteria =\> exaggerated immune response =\> Tissue damage and ulcers
66
What is the disease response process in Oral Lichen Planus?
Epitope spreading:
Initial T cell response causes lesions in keratin in the oral and conjunctival mucosa =\> Basement membrane disruption reveals new Ag =\> secondary response causes blistering in secondary pemphigoid
67
What is the first test you would get for a pt with suspected lupus, Sjogren syndrome, or systemic sclerosis?
Anti-nuclear antibody (ANA)
(sensitive test for multiple autoimmune diseases, can prompt more specific testing to confirm Dx)
68
An ANA immunofluorescent stain comes back with a homogeneous appearance on the cells. what disease process is most likely?
Systemic Lupus Erythematosus (SLE)
69
What is the gene associated with SLE?
HLA-DQ
70
What populations are affected by SLE?
Female
Family hx of SLE
People who are chronically exposed to UV light
71
Pt presents with malar rash, fever, fatigue, and edema in the legs. Upon testing, pt has hemolytic anemia and a positive ANA. What disease does she most likely have?
SLE
72
What are the most common signs and symptoms of lupus? (a lot)
Malar rash
Hair loss
Swollen LNs
Chest pain
Muscle aches
Inflammation and damage to kidneys, lungs, heart, BVs, CNS
Raynaud's in fingers and toes
Arthritis/joint pain
Fever, fatigue
photosensitive
Anemia
73
What stage do people normally present to their physician with Lupus Nephritis? What is the terminal stage of lupus?
Typically present with diffuse lupus nephritis
Sclerosing nephritis (fibrotic) is terminal
74
What is the appearance of the glomeruli in diffuse Lupus Nephritis (IV)?
Increased proliferation of endothelial, mesangial, and epithelial cells
Immune deposits in the subendothelium (grainy/granular IF appearance as in a Type III Hypersensitivity due to IgG ab-containing complexes)
75
What occurs in Libman-Sacks Endocarditis? What disease is this a complication of?
"Verrucous" (warty) valve deposits composed of fibrin
Not infective
Can embolize (rarely)
Complication of SLE
76
What type of cell seen in SLE is seen as a neutrophil/macrophage ingesting the nucleus of a damaged cell?
L-E cell
May be seen in blood/body fluids
77
What are the main diagnostic features of Discoid Lupus Erythematosus?
Discoid rash
Positive ANA
Positive immunofluorescence
Negative Anti-DS DNA
78
What are the main diagnostic features of Drug-Induced Lupus Erythematosus?
Arthralgias (joint aches/fever)
Positive ANA
Discoid rash
Hematologic disease
Positive immunofluorescence
79
What type of lupus is associated with a positive Anti-Histone Ab?
Drug-Induced Lupus
80
What drugs cause Drug-Induced Lupus? What genes do they interfere with?
Hydralazine (anti-arrhythmic) - HLA-DR4
Procainamide (BP med) - HLA-DR6
81
What glandular tissue is targeted in Sjogren syndrome?
Lacrimal and salivary glands
82
What is the clinical presentation for Sjogren syndrome?
Dry, irritated "gritty" eyes
Dry mouth (xerostomia) =\> yeast infection and root caries
83
What Ab are tested for in Sjogren syndrome?
Anti-Ro/SS-A
Anti-La/SS-B
84
What are the main complications of Sjogren syndrome?
Formation of extraglandular tissue - pulmonary fibrosis
Lymphoid proliferation becoming clona =\> lymphoma
85
How does systemic sclerosis present on a histological slide?
Dense collagenous deposition
Vascular hyalinization
86
Why does systemic sclerosis cause raynaud's phenomena?
Sclerosis of the vasculature in the fingers cuts off blood supply =\> necrosis
87
How does the ANA immunofluorescent pattern present in systemic sclerosis?
Speckled
88
How does the ANA immunofluorescent pattern present in CREST syndrome?
Centromeric
(Ab attack the centromeres of the cells)
89
What does CREST syndrome encompass?
C - Calcinosis/calcium deposits in the skin
R - Raynaud's phenomenon (spasm of BVs in response to cold or stress)
E - Esophageal dysfunction =\> acid reflux
S - Sclerodactyly: thickening and tightening of skin on fingers and hands
T - Telangiectasias: dilation of capillaries causing red marks on surface of skin
(better prognosis than diffuse sclerosis)
90
What are the hallmarks for Mixed Connective Tissue Disease?
High titer for Anti-ribonucleoprotein (RNP)
Commonly presents w/ raynaud's phenomenon
91
What are the IgG4-related diseases?
Autoimmune pancreatitis
Riedel thyroiditis
Mikulicz's syndrome (autoimmunity of salivary glands)
Idiopathic retroperitoneal fibrosis (in ureters =\> kidney failure but it is all up and down the retroperitoneum)
Inflammatory pseudotumors
Inflammatory aortitis
92
What is the pathophysiology of IgG4 related disease?
IgG4-producing plasma cells, T lymphocytes causing irreversible tissue damage and fibrosis
93
What is the main process behind transplant rejection?
Allorecognition (body recognizes transplant as non-self)
94
How does the direct pathway of allorecognition affect tissue graft?
Dendritic cells in the donor organs become APCs for initiating anti-graft response
95
How does the indirect pathway of allorecognition affect tissue grafts?
Recipients APC recognize MHC Ag on graft donors and present this Ag to its own CD4 cells =\> activate macrophages or B cells =\> plasma cells to attack BVs
96
When does hyperacute graft rejection occur?
Minutes to hours
Recipient has pre-formed Ab to the donor tissue =\> inflammation followed by thrombotic microvasculopathy
97
What is the breakdown product in Acute Ab-mediated tissue rejection?
Complement C4d breakdown product
98
When does acute cellular tissue rejection occur? What are the mediators of this process?
Days, months, years of transplant
T-Cell mediated
99
What drugs are used to prevent Ab-mediated rejection of transplatns?
Immune globulin
Rituximab (anti CD20 recombinant Ab)
100
What is the drug used to treat T-lymphocyte mediated cellular rejection?
Tacrolimus
101
What infections are transplant pts at higher risk for?
Viral: Polyomavirus, cytomegalovirus
Fungal
Bacterial
102
What types of tumors are transplant pts at increased risk for?
Viral-induced tumors: lymphomas, Kaposi sarcoma
Squamous cell carcinoma (skin)
103
Graft Vs Host Disease is mediated by what cells?
T Lymphocytes
104
What are common infectious consequences of B cell deficiencies?
Pyogenic bacterial infections
Enteric bacterial and viral infections
105
What are common infectious consequences of T cell deficiencies?
Viral and other intracellular microbial infections (pneumocystitis jiroveci)
Some cancers (EBV-associated lymphomas, skin cancers)
106
What is defective in Chediak Higashi syndrome?
Failure of phagolysosomal fusion =\> Increased bacterial infections
(AR primary leukocyte disorder, fatal w/o stem cell transplant)
107
Defects in melanocytes leading to albinism in pts and a giant granule appearance on histological slides can be indicative of what disorder?
Chediak Higashi syndrome
108
What mechanism is defective in chronic granulomatous disease?
Failure of superoxide production w/in phagocytes =\> accumulation of macrophages =\> wall off infection
(primary leukocyte disorder)
109
Failure of what components cause MAC deficiency? What infections does this commonly lead to?
Deficiency in C5, 6, 7, 8, 9
Neisseria infection =\> meningitis
110
Hereditary angioedema is caused by deficiency in what?
C1 inhibitor
| (AD inheritance)
111
What enzyme is most commonly defective in AR-inherited SCID?
Adenosine deaminase deficiency
112
What is defective in X-Linked SCID?
Mutations in IL receptors =\> reduced # of T cells
113
What is deficient/failed in DiGeorge syndrome?
Failure of pharyngeal pouches 3 and 4 =\> failure of development of thymus, parathyroids, heart, and great vessels =\> Deficient in mature T lymphocytes
114
What chromosome has been deleted to produce DiGeorge syndrome?
22q11
115
What disease process can result in Tetralogy of Fallot, truncus arteriosus, and tetany?
DiGeorge Syndrome
116
What enzyme is deficient in X-linked agammaglobinemia?
Bruton tyrosine kinase (gene defective on X chromosome) =\> Inability of B cells to mature
117
What infections are pts with agammaglobulinemia susceptive to?
Encapsulated bacteria: Strep pneumoniae, haemophilus influenzae Type B, streptococcus pyogenes, pseudomonas aeruginosa, staph aureus
Viruses
Protozoa: giardia lamblia
118
What failed in Hyper IgM syndrome?
CD40/CD40L mutations =\> interfere w/ T cells helping B cells to class switch
119
What is the most common significant primary immunodeficiency?
Common Variable Immunodeficiency (CVID) - disease of exclusion
120
How do pts with CVID present?
Older pts (after months after birth)
Recurrent encapsulated bacterial infections (sinus and pulmonary infections)
Granulomas
Chronic diarrhea (giardia lamblia)
Autoimmune disease: anemia, thrombocytopenia
121
Pt presents with an anaphylactic reaction after a red cell transfusion. He states he has a history of frequent infections and allergies. What does this patient most likely have?
IgA deficiency
122
What gene is mutated in Wiskott Aldrich syndrome? What sx are characteristic?
WASP gene mutation
Triad of sx: thrombocytopenia, eczema, recurrent infections
123
What is deficient in Ataxia Telangiectasia?
ATM gene mutation =\> defective gene repair =\> immune deficiency (def IgA and IgG) =\> resp infections, autoimmune dz, CA
124
AIDS is the manifestation of when HIV affects immune function to the point of what 3 things?
1. Opportunistic infections
2. Secondary neoplasms
3. Neurologic manifestations
125
Who are the at-risk populations for HIV?
Homosexual/bisexual men
IV drug users
Hemophiliacs
Other recipients of blood/blood components
Heterosexual contacts of above groups
Newborns in areas with high female HIV prevalence
126
What is the capsid protein tested for in HIV?
P24 (the 2nd detectable substance for HIV)
127
What are the glycoproteins important for HIV attachment to cells? What can they be used as?
GP120 and GP41
Good drug/vaccine targets
128
What are the major regions of the HIV-1 genome to know? What do they encode?
Long terminal repeat (LTR): initiates txn, binds txn factors
GAG: encodes ptn **inside** virus
ENV: encodes for **surface glycoptns**
Pol: encodes viral enzymes (polymerase)
129
Life cycle of HIV
1. Virus entry using CD4 molecule as a receptor (co-receptors may include CCR5 and CXCR4)
2. GP120 binding =\> conformational change
3. GP120, CD4 bind CCR-5
4. GP41 membrane penetration
5. Membrane fusion =\> entry of viral genome into cytoplasm
6. Reverse transcriptase-mediated synthesis of proviral DNA
7. Integration of provirus into host cell genome via integrase =\>
8. Host cell activation =\> LTR initiates TXN
9. Synthesis of HIV ptns
10. Budding and release of mature virion
130
In the case of HIV, why is antigenic stimulation counter-intuitive to the host immune response?
Ag stimulation is supposed to release NFkB =\> upregulate the T cell response but actually initiates viral txn through the LTR
131
What is the direct cytopathic effect in HIV?
Viral replication in the cell is responsible for host cell/CD4 death
132
What is pyroptosis?
Inflammasome-mediated programmed death pathway responsible for cell death in non-replicating viral infection
133
How does HIV tropism affect macrophages?
Macrophages become HIV reservoir and become resistant to cytopathic effects
134
How does HIV tropism affect DCs?
Mucosa - used for transport to LNs
LNs: additional reservoirs for HIV
135
How does HIV tropism affect microglia?
Infection in monocytes to microglial cells in brain allows HIV access to CNS
Neuronal damage from viral product
136
What happens to B lymphocytes in HIV infection?
Proliferative response (might be due to secondary infection)
May become clonal (lymphoma)
Non-specific hypergammaglobinemia
Impaired humoral immunity
137
How long is the acute viremic period of HIV?
2-3 weeks
138
When does the the acute retroviral syndrome spike of HIV occur? What occurs during this phase?
3-7 weeks after infection
Seroconversion - developing anti-HIV Ab
139
What is the sequence of detectable substances in HIV testing?
1st detected: Viral RNA via Nucleic Acid Test (NAT)
2nd detected: Ptn Ag p24
3rd: HIV Ab
140
What is the window period for HIV testing?
The period of time (7-14 days) that it takes to test donated blood and blood products for HIV infection
141
What is the clinical signifiance of the viral set point?
Signifies the end of the initial viremic spike
May predict the CD4 cell loss and latency period
142
What diseases manifest in AIDS?
Opportunistic infections (pneumocystis PNA, TB, toxoplasma, candida mucositis, cryptosporidium diarrhea)
Neoplasia (kaposi sarcoma, lymphoma)
143
What opportunistic fungal infection is the AIDS defining illness?
Pneumocystis jiroveci (carinii)
144
What virus (along with HIV) is associated with the development of Kaposi sarcoma?
HHV 8 (EBV reactivated)
145
How do AIDS lymphomas develop?
HIV allows opportunistic viral infection (EBV reactivation)
HIV decreases cell immunity which usually checks B cell proliferation
146
What CA is AIDS-defining?
Cervical CA (infection by HPV)
147
What are the systemic amyloidoses and their associated fibril ptn?
Immunocyte dyscrasias w/ amyloidosis (primary) - AL
Reactive systemic amyloidosis (secondary) - AA
Hemodialysis-associated amyloidosis
148
What are the hereditary amyloidoses and their associated fibril ptn?
Famiial Mediterranean fever - AA
Familial amyloidotic neuropathies - ATTR
Systemic senile amyloidosis - ATTR
149
What are the localized amyloidoses?
Senile cerebral - Alzheimer's
Endocrine - Type 2 DM
Medullary carcinoma of thyroid
Islets of langerhans
Isolated atrial amyloidosis
150
What is the initial presentation of amyloid in the kidney?
Edema due to disruption of glomeruli and resulting proteinuria
151
What is the initial presentation of amyloid in the heart?
Dysrhythmias due to disruption of myocardium
152
What stain is used to demonstrate presence of amyloid? What color will it appear as?
Congo red stain
Appears apple green
153
What Ab are tested for in lupus?
Anti DS DNA
Anti Smith
154
What Ab are tested for in systemic sclerosis?
Anti-DNA Topoisomerase (Scl-70)
155
Failure of immune cell development in what structure leads to X-linked agammaglobulinemia?
Bone marrow
156
Failure of immune cell development in what structure leads to ADA deficiency, X-linked SCID, DiGeorge, MHC class II deficiency?
Thymus
157
Failure of immune cell development in what structure leads to CVID, Hyper-IgM syndrome, IgA def?
Blood circulation
158
What are the most common locations of amyloid to manifest?
Brain
Kidney
Liver
Heart
Fat pads
