Host Defense Practice Exam 2

thickening of the intima occurs along with the fibrotic processes of chronic rejection

Auto-antibody (against type IV collagen in kidneys, lungs)

"prepared mind syndrome" - discovered that patient didn't produce type IV collagen because his tissues didn't cause reaction when exposed to Goodpasture serum (Goodpasture is atopic -- serum should cause the same problem when inserted into an unaffected individual)

C5a-9 all form the membrane attack complex that makes a membrane pore
C3b coats antigen (opsonization)
C3a, C4a, and C5a are all anaphylatoxins
C5a is a chemoattractant for neutrophils, eosinophils, basophils and monocytes (think "Chanel #5")

Early exposure to childhood illnesses may "set" normal Th1 and Th2 responses to subsequent environmental antigen exposure. Allergies are rarer in large families and with early day care. Lack of early exposure to infectious Ag and underproduction of Tregs are associated with risk of developing allergies.

Bone marrow transplant: graft-versus-host disease

B - polyclonal, not monoclonal ("frustrated" B-cells )
c - Type III, not Type I
d - both platelets and fibrin are found where an IC binds to FcgR on vascular endothelium

CD59 prevents C8/9 association and pore assembly of MAC
Factor H, Factor I and CD46 all regulate C3b's C5 convertase activity
Factor I and CD46 regulate C4b's C3 convertase activity
CD55 regulates C3 convertase in all pathways by accelerating decay (think "55 raises speed-limit"
C1 INH, in classical pathway, dissociates C1r and C1s from C1q

A - UVB light (not UVA) stimulates antigen presentation
B - estogen increase likelihood of developing autoimmune disorders (likelihood is highest between puberty and menopause)
C - accumulation of ICs cause all of these problems (high FcR concentration in skin and kidney)
D - SLE is an example of Type III hypersensitivity (IC disease)

Tregs (regulatory T cells) play a crucial role in immune regulation by suppressing excessive immune responses. They achieve this through various mechanisms such as competition with other immune cells, inhibiting dendritic cells (DCs), secreting TGF-B (transforming growth factor-B), and inhibiting T-cell activation. However, Tregs do not secrete INF-g (interferon-gamma), which is a cytokine produced by other immune cells to enhance immune responses. Therefore, the correct answer is "Secreting INF-g."

M-cells transport antigens from the lumen of the GI tract and the bronchioles

lack of early classical components (C1, C2, C4) won't lead to overwhelming infection, but will decrease IC clearance and lead to IC disease

TMMI response will not help reduce the effects of the toxins

Basophils circulate; mast cells reside in tissue sites

An adjuvant is a substance that is added to a vaccine to enhance the immune response to the antigen. In this case, the adjuvant is described as a peptide that is attached to a polysaccharide antigen. The role of this adjuvant is to help induce a T-dependent response, which means it activates T cells to recognize and respond to the antigen. By doing so, it helps in the development of memory cells, which provide long-term immunity against the antigen.

Corticosteroids act by inhibiting the production of pro-inflammatory cytokines during the late reaction of an allergic response. Pro-inflammatory cytokines are molecules that promote inflammation and immune responses. By inhibiting their production, corticosteroids help to reduce inflammation and alleviate symptoms associated with allergies. This action occurs during the late phase of the immune response, which is characterized by the release of cytokines and the recruitment of immune cells to the site of inflammation.

All three pathways involve activity of C3 convertase and C5 convertase

The only treatment "routinely" available for SCID is bone marrow/stem cell transplantation.

Systemic Lupus - Type III, immune complex hypersensitivity (inability to properly dispose of IC)
Allergic Rhinitis - Type I, IgE mediated allergy
Goodpasture's Syndrome - Type II, auto-immunity to type IV collagen
A positive TB skin test - Type IV, TMMI -> granuloma
Grave's Disease - Type II, auto-antibodies to TSH receptor -> hyperthyroidism

B, C and E are all true, but they are not the major clearance mechanisms.

Immature dendritic cells take up commensal bacteria, give weak signals to induce regulatory T-cell formation (inhibiting immune response and developing tolerance to the commensal bacteria). Destruction of commensal bacteria (eg. by antibiotics) allows pathogens (eg. clostridium difficile) to penetrate epithelial cells, bind to dendritic cells, make them mature and form immune response.

The rare gamma-delta T-cell lymphoma found in SCID gene transfer patients is caused by the point of insertion of the viral vector. When gene transfer is used as a treatment for SCID patients, a viral vector is used to insert the corrected gene into the patient's cells. However, in some cases, the point of insertion of the viral vector can disrupt the normal functioning of the cells and lead to the development of lymphoma.

When a person is stung by a bee for the second time and develops urticaria, it indicates an allergic reaction. In this case, both IgE and IgG antibodies are being produced against the bee venom antigen. While IgE is the primary antibody involved in allergic reactions, the presence of IgG suggests a secondary immune response. This inappropriate immune response to bee venom can lead to symptoms such as urticaria.

When an antigen is consumed orally, the key feature that distinguishes the induction of a response and the induction of tolerance is inflammation. Inflammation is a natural response of the body to infection or injury, and it involves the release of various immune cells and molecules to fight against pathogens. In the case of consuming an antigen, if inflammation occurs, it indicates that the immune system is recognizing the antigen as a threat and will mount a response against it. On the other hand, if there is no inflammation, it suggests that the immune system is tolerating the antigen and not initiating a response.

The correct answer is "Subcutaneous mycoses in adulthood". Selective IgA deficiency is a condition where the body lacks or produces very low levels of immunoglobulin A (IgA). This deficiency can result in various symptoms, including a family history of IgA deficiency or agammaglobulinemia, a high incidence of oral infections, frequency of respiratory infections, and chronic diarrhea. However, subcutaneous mycoses, which are fungal infections that affect the skin and underlying tissues, are not typically associated with selective IgA deficiency.

need TMMI for intracellular pathogen

An allergic reaction occurs when the immune system becomes sensitized to a specific allergen. Sensitization refers to the initial exposure to the allergen, which triggers the production of specific IgE antibodies. These antibodies bind to mast cells and basophils, leading to their activation. When the allergen is encountered again, it binds to the IgE antibodies on mast cells and basophils, causing the release of inflammatory mediators such as histamine. This results in the symptoms of an allergic reaction. Therefore, a sensitization event is an absolute requirement for an allergic reaction to occur.

Bacterial superantigen binds to alpha chain on MHC class II and B chain on TCR.
Superantigens are found in unprocessed form; are not bound to conventional antigen-binding site.

Arthus reactions are so large because a large amount of preexisting antibodies complex to form IC with the antigen. In a normal response, there's a delay in IC formation while B-cells produce antibody. In both situations, IC activates neutrophils via FcR and CR1. Activated neutrophils release IL-8 which recruits more neutrophils to the site. A painful inflammatory response occurs, and excess IC are carried to the liver bound to erythrocytes via CR1 receptors. In an Arthus reaction, CR1-medicated IC disposal is immediately overwhelmed.

In this scenario, the malfunction of the immune system occurs when chemokines secreted by the tumor induce a Th0 cell to transform into a Treg cell. Treg cells are regulatory T cells that suppress the immune response, providing protection for the tumor. This malfunction allows the tumor to evade destruction by the immune system. The other options do not directly relate to the immune system failing during response to a tumor antigen.

All of the others promote a Th1 response; don't want to suppress Th1 response with IL-10.

Serum IgA is mostly monomeric, while secretory IgA is mostly dimeric (joined by J chain). The production of sIgA requires plasma cells of lamina propria AND epithelial cells of mucosa.

FDC is an antigen-retaining cell with Iccosomes on it; FDCs seem to be derived from reticular stromal cells

T-cells at autoimmune sites are producing IL-17 (not INF-gamma). The transcription factor for Th17 is Ror. DCs at these sites produce IL-23 and IL-6, not IL-12. T-Bet is a Th1 transcription factor. GATA3 is a Th2 transcription factor.

Mast cells don't contain thrombopoeitin, which would cause hematopoietic stem cells to form platelets and contribute to blood clotting. Mast cells do not promote clotting at all; they oppose it by secreting heparin.

Mast cells do contain histamine, heparin, GM-CSF and TNF-alpha

Virus would induce CD4, 25 Tcell proliferation to block immune response against it, but by upregulating TGF-B. Viruses *do* produce soluble cytokine receptors.

Patients with CVI have lots of B-cells, and no or very low IgG. The IgG itself is not abnormal; the levels are abnormally low. Terminal B-cell differentiation is defective, plasma cells do not form, and antibodies are not produced.
This is different from X-linked agammaglobulinemia, in which there is a defect in EARLY B-cell development and there are few or no B-cells present (therefore no plasma cells, no Ig of any kind)

The given answer is "none of the above" because all of the options listed are reasons why there is a wide disparity of symptoms experienced by a large population of humans after being infected with a virus. Some individuals may have too few or mutated TLRs, inherent polymorphism is found at each level including MHC, TLR, cytokines, and DCs, having the "wrong" TLR can cause an ineffective or pathologic response, and having too many TLRs can create a hyper-response and cause collateral damage. Therefore, none of the options can be excluded as a reason for the wide disparity of symptoms.

A - due to HYPERacute hypersensitivity
B - patient developing IC disease may just be responding to immunization
C - Anti-C3b and anti-IgG are both used to identify ICs in tissue biopsies

all other choices are associated with late response

Monoclonal antibodies have been used to treat Rheumatoid Arthritis, Allergies, Transplantation rejection, and B-cell antibody mediated diseases (B lymphoma). However, Hashimoto's disease, an autoimmune disorder affecting the thyroid gland, has not been thought to be controlled by the use of monoclonal antibodies. Monoclonal antibodies are typically used to target specific proteins or cells involved in the disease process, and in the case of Hashimoto's disease, the underlying mechanism does not involve a specific protein or cell target that can be effectively treated with monoclonal antibodies.

CCL19 and CCL21 attract T-cells, not B-cells.

Serum tryptase (measure of mast cell activation/degranulation) and skin tests are an INDIRECT measure of antigen/antibody system and antibody isotypes. Skin tests may be dangerous if the patient is highly reactive.

A - in secondary immune response, IgG level is elevated but is never higher than albumin level
B - in SLE, the patient makes antibodies against their actual DNA, not proteins encoded in their DNA
C - the spleen doesn't phagocytize the increased ICs formed during IC disease
D - Serum from a patient with a chronic infection would have increased polyclonal IgG (not IgE) antibodies

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