By I. Lim Jennifer
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Extra info for Age-Related Macular Degeneration, 2nd Edition
Scavenging macrophages may become APCs at the site, serving to restimulate recruited T cells thereby activating the effector phase of the immune response. Immune responses to bacterial or viral antigens, especially chlamydial HSPs, trapped in tissues after occult infection may also stimulate antigen-speciﬁc immunity, or autoimmunity by cross-reactive molecular mimicry (133). Alternatively, T cells may be recruited by innate responses and become activated by antigenindependent bystander mechanisms.
The RPE express speciﬁc and nonspeciﬁc complement inhibitors such as decay accelerating factor and vitronectin to suggest intrinsic defense mechanisms to prevent against complementmediated injury (183). Ocular Immune and Inflammatory Disorders Resulting in Atrophic Retinal Degeneration or CNV Ocular Histoplasmosis Syndrome OHS may represent a condition to suggest a role for infection-triggered immunity as a mechanism for RPE injury and CNV formation. The syndrome is presumed to be induced by the inhalation of live histoplasmosis capsulatum, which infects the lung and hilar lymph nodes (184).
These cells remove the offending stimulus in a nonspeciﬁc manner via phagocytosis or enzymatic degradation. The key concept is that the stimuli of innate immunity interact with receptors on monocytes, neutrophils, or parenchymal cells that have been genetically predetermined by evolution to recognize and respond to conserved molecular patterns or “motifs” on different triggering stimuli. These motifs often include speciﬁc amino acid sequences, certain lipoproteins, certain phospholipids, or other speciﬁc molecular patterns.
Age-Related Macular Degeneration, 2nd Edition by I. Lim Jennifer