This is the practice exam sent out for the second Host Defense test.
C9; membrane pore formation
C3b; pathogen opsonization
C3a; anaphylatoxin
C4a; binding to erythrocyte for IC removal
C5a; chemoattractant for leukocyte recruitment
Factor H
Factor I & CD 46
CD 55
CD 59
C1 INH
Classical pathway only
MB-Lectin pathway only
Alternative pathway only
Both classical and MB-Lectin pathways
Classical, MB-Lectin and alternative pathways
Immune complex disease
Bacterial infections, particularly in childhood
Infection by pyogenic bacteria and Neisseria spp.
Infection by Neisseria spp. only
Infection by pyogenic bacteria only
Serum IgA is primarily dimeric
Secreted mucosal IgA is mostly monomeric
The production of sIgA requires only the epithelial cells of the mucosa, not the plasma cell epithelium
SIgA contains a component of pIgR that is bound covalently
Dimeric IgA has no J chain
Desensitization
Commensal bacterial development
Dendritic cell inactivation
Inflammation
Mucosal epithelium leakiness
A family history of IgA deficiency of aggamaglobulinemia
A high incidence of oral infections
Frequency of respiratory infections
Chronic diarrhea
Subcutaneous mycoses in adulthood
Promote the colonization of pathogenic bacteria in the guyt
Thrive with antibiotic treatment
Inhibit regulatory T cells
Are not involved in mucosal tolerance
Prevent the differentiation of immature dendritic cells to mature dendritic cells
Maternal antibody is inactivated in children with SCID; antibody administration is too risky
SCID involves a defect with both B & T cells; administering pooled antibodies does not solve the T-cell defect
SCID involves a defect with only T cells; administering pooled antibodies does not solve T-cell related defects
SCID patients have B-cells that are functional but they do not develop; administering pooled antibodies does not stimulate these faulty B-cells
Maternal antibody does help the SCID patients and IgG pooled antibody is the preferred treatment choice
Patient has increased number of lymphocytes and produces abnormal IgG
Early B-cell development is normal but there is a marked reduction in terminal B-cells, plasma cells and reduced numbers of germinal centers
On an FACS analysis, you not normal or normal high levels of B-cells
CVI could involve inappropriate inhibition of B-cells by CD4, 25 FoxP3 cells
Defects may reside in defective cytokine signaling or cross-talk between B and Th2 cells
The point of insertion of the viral vector leads to the lymphoma
The pathology of SCID leads to the lymphoma
A failed bone marrow transplant leads to the lymphoma
An uncontrolled TMMI response leads to the lymphoma
HLA antigen incompatibility leads to the lymphoma
Erythrocytes are needed to take excess IC to the liver for disposal
Activated neutrophils release IL-8
Preexisting antibodies complex with antigen
Antigen-antibody complexes interact with both FcR and CR1 on neutrophils
Painful inflammation results
They travel unbound in the blood to the liver.
They are bound to CR1 receptors on vascular endothelium and cause vascular inflammation
They travel bound to erythrocytes in the blood to the spleen
They travel in the circulation to the liver bound to CR1 receptors on blood cells
They are degraded at the site of inflammation
Systemic Lupus
Allergic Rhinitis
Goodpasture's Syndrome
A positive TB skin test
Grave's Disease
Competition
Inhibition via DCs
Secreting TGF-B
T-cell inhibition
Secreting INF-g
Is defined as accelerated rejection taking place within 48 hours of the transplantation
Arteriolar narrowing due to an increase in the thickness of the intima
Is mediated by recipient alloantibody directed against donor antigens that were present prior to transplantation
Transplantation of an A, B or AB organ into an "O" individual
Widespread vascular injury
Hyperacute rejection
Bone marrow transplant
Acute rejection
Chronic rejection
Xenotransplant rejection
The development of swelling, redness and throbbing pain in the patient's arm 8 hours after receiving a tetanus shot for the second time in a month is an example of acute hypersensitivity
If a patient develops Immune Complex disease, this is a definite sign that the patient has a bacterial infection
Peroxidase or immunoflorescent labelled anti-IgG, but not anti-C3b, are reagents used to identify ICs in a tissue biopsy
Binding of the IC to endothelial CR1 receptors results first in production of cytokines and next in attraction of neutrophils to the site of binding
None of the above
UVA light is especially influential in stimulating antigen presentation by dendritic cells of the skin
Postmenopausal women have a higher likelihood of developing autoimmune disorders due to their decreased estrogen levels
Patients with systemic immune complex disorders like SLE (systemic lupus erythomatus) often present with skin rashes, glomerular nephritis and joint pain
SLE is an example of Type II hypersensitivity
None of the above
In secondary immune responses the level of IgG in a patient's serum is always greater than the level of albumin
In SLE, the patient makes antibodies against proteins encoded in their DNA
Spleenomegaly develops as a result of the spleen's attempt to phagocytize the increased number of antibody-antigen complexes formed during IC disease
Serum from a patient with a chronic infection would have significantly increased levels of polyclonal IgE antibodies
None of the above
Type I
Type II
Type III
Type IV
Serum sickness is an example of a systemic, rather than local, immune response
Persons with chronic infections usually have monoclonal hypergammaglobulinemia
Glomerular nephritis, thyroiditis, and juvenile rheumatoid arthritis result from Type I hypersensitivity responses
Platelets, but not fibrin, are found where an IC binds to FcgR on vascular endothelium
None of the above
Both constitutively express high affinity Fce receptors
Both have cytoplasmic stores of vasoactive mediators
Both develop from hematopoietic precursors
Both reside in tissue sites
Both have cytoplasmic granules
Histamine
Heparin
Thrombopoietin
GM-CSF
TNF-a