2011-2012 Basic and Clinical Science Course, Section 9: by Ramana S. Moorthy MD

By Ramana S. Moorthy MD

Starts with an in-depth evaluate of immunemedicated eye ailment, summarizing easy immunologic recommendations, ocular immune responses and particular issues in ocular immunology. Discusses the scientific method of uveitis and experiences noninfectious (autoimmune) and infectious sorts of uveitis, with an multiplied part on viral uveitis and new fabric on infectious and noninfectious scleritis. better detection of infectious brokers by way of immunologic and genetic equipment and new biologic therapeutics are particular. additionally covers endophthalmitis, masquerade syndromes, issues of uveitis and ocular facets of AIDS. encompasses a variety of new colour photographs. significant revision 2011-2012

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Extra info for 2011-2012 Basic and Clinical Science Course, Section 9: Intraocular Inflammation and Uveitis (Basic & Clinical Science Course)

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Rarely, if adequate free toxin is present, IgG antitoxin immune complexes can form and mediate inflammation . However, if most of the antigen has been cleared, then the primed T lymphocyte may enter the skin but become inactive, retaining memory, or the T lymphocyte may exit the skin through afferent lymphatics to reenter the lymph node. Similarly, antibodies or antibody-producing B lymphocytes may remain in the skin or reach the lymph nodes. CHAPTER 2: Immunization and Adaptive Immunity. Secondary response to poison ivy toxin The immunologic mechanisms work much faster after the second encoun ter with poison ivy toxi n.

Forming a unique epitope. The combination of peptide and HLA protein is recognized by T-Iymphocyte receptors CD4 and CD8. thereby beginning the activation process of adaptive immunity. Different HLA molecules vary in their capacity to bind various peptide fragments within their groove. and thus the HLA type determines the repertoire of peptide antigens capable of being presented to T lymphocytes. Specific HLA alleles are important risk factors for certain forms of uveitis. See Chapter 4 for a more thorough discussion of HLA molecules and disease susceptibility.

Especially in the processing and effector phases. offer partial explanation. During the processing phase of the primary response. 000) and then stimulate these cells from a completely resting and naive state. a sequence that requires days. The secondary processing response for T and B lymphocytes is shorter for at least 3 reasons: • Upon removal of antigen. T and B lymphocytes activated during the primary response may gradually return to a resting state. but they retain the capacity to become reactivated within 12-24 hours of antigen exposure.

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