Complexes of IgG bound to soluble multivalent antigens can activate the classical pathway on the complex, targeting it for of complement, resulting in the deposition of endocytic uptake by cells bearing. Select one: a. C4b; CR2 and Fc receptors b. c. C5-9; CR1 and Fc receptors d. C3b; CR1 and Fc receptors e. C2a; CR2 and Toll-like receptors C3b; CR2 and Toll-like receptors

Individuals with allergies often mount IgE antibody responses to non-infectious environmental antigens. Examples are peanut allergies, allergies to house dust mites, and allergic responses to bee stings. In all of these cases, the allergic response is mediated by the cross-linking of the high affinity IgE receptors on mast cells (FceRI) which are pre-bound to the allergen-specific IgE antibodies. Yet, the symptoms of these different allergic responses can vary greatly, and can include skin rashes or hives, swelling of the throat and difficulty breathing, to gastrointestinal symptoms such as cramps, diarrhea or vomiting. How can different IgE-mediated allergic responses cause such different symptoms?

To study the immune responses that provide protection against tumor growth in mice, some investigations have used the EL4 mouse thymoma line. This tumor cell line was derived from a C57BL/6 mouse, and represents a type of T cell lymphoma. When transplanted into Rag-deficient mice, the mice rapidly succumb to the tumor. This is also the case when the mice receive wild-type C57BL/6 T cells the day before tumor cell injection. However, Rag-deficient mice were protected when the transferred T cells came from mice that lacked expression of one cytokine receptor, as shown in the fugure below.  Name one likely candidate for the cytokine receptor that is knocked out in the T cells that are able to protect the mice.

When T cells are activated by recognizing peptide:MHC complexes on dendritic cells in the lymph node, they up-regulate the receptor CD69. For T cells expressing a given T-cell receptor, the initial strength of the T-cell receptor signal can be modulated by varying the number of peptide:MHC complexes on the dendritic cells, or by varying the affinity with which the T cell-receptor binds to the peptide:MHC complexes. As a result, T cells stimulated with stronger T-cell receptor signals will maintain high expression of CD69 for one or two days longer that if those same T cells were stimulated with weaker T-cell receptor signals. Therefore, T cells stimulated with weaker T-cell receptor signals are likely to: Die by apoptosis Undergo more rounds of proliferation that T cells stimulated with stronger T-cell receptor signals Migrate to the B-cell zones of the lymph node Have reduced effector functions, such as cytokine production Egress from the lymph node 1–2 days earlier than T cells…