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Untitled - D Ank Unlimited

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ontogeny 542 oral immunology<br />

ontogeny<br />

The development of an individual organism from conception<br />

to maturity.<br />

open reading frame (ORF)<br />

A length of RNA or DNA that encodes a protein and may<br />

signal the identification of a protein not described previously.<br />

An ORF begins with a start codon, ends at a stop<br />

codon, and lacks a termination codon.<br />

opisthorchiasis (clonorchiasis) immunity<br />

Antibodies synthesized in patients with opisthorchiasis (or<br />

chlonorchiasis) react with the various developmental stages<br />

of the parasites. Stage-specific and cross reactive common<br />

antigens have been detected and identified. Immunoglobulin<br />

G (IgG) is the predominant class of antibodies in serum,<br />

but IgE has also been detected to a lesser degree. The bile<br />

contains secretory IgA as the principal immunoglobulin.<br />

The parasite antigens manifest IgE-potentiating activity.<br />

Although high antibody titers are achieved in infected<br />

patients, their protective ability is doubtful. Some investigations<br />

have suggested that complement-fixing antibodies may<br />

play a role but Opisthorchis may be able to activate complement<br />

by way of the alternative pathway leading to lymphocyte<br />

killing. Cell-mediated immunity also occurs following<br />

natural infection or immunization with the parasite antigen.<br />

The role of T cells remains to be determined. Primary<br />

infection does not appear to protect against reinfection by<br />

the same parasite. Thus, there appears to be a lack of protective<br />

acquired immunity. The liver flukes survive in the<br />

biliary system that may serve as a type of immunologically<br />

privileged site. These parasites can shed their surface teguments<br />

following injury by immune mechanism, representing<br />

yet another mechanism to evade host defenses.<br />

opportunistic infection<br />

An infection produced by microorganisms that are usually<br />

of relatively low virulence but become more aggressive in<br />

subjects with altered or defective cell-mediated immunity.<br />

Susceptible individuals include individuals with acquired<br />

immune deficiency (AIDS) and severe combined immunodeficiency<br />

(SCID) and organ transplant recipients. Typical<br />

microorganisms producing opportunistic infections include<br />

Pneumocystis carinii, Candida albicans, Mycobacterium<br />

avium intracellulare, Cryptosporidium, Toxoplasma, cytomegalovirus,<br />

and herpesvirus.<br />

opportunistic pathogen<br />

A microorganism that produces disease only in persons<br />

whose immune defense mechanisms are compromised as in<br />

AIDS.<br />

opsonin<br />

A substance that binds to bacteria, erythrocytes, or other<br />

particles to increase their susceptibility to phagocytosis.<br />

A host protein that coats a pathogenic microorganism or<br />

macromolecule to make it bind more readily to phagocyte<br />

receptors, thereby enhancing phagocytosis. Opsonins<br />

include antibodies such as IgG 3, IgG 1, and IgG 2 that are<br />

specific for epitopes on particle surfaces. Following interaction,<br />

the Fc region of the antibody becomes anchored to<br />

Fc receptors on phagocyte surfaces, thereby facilitating<br />

phagocytosis of the particles. In contrast to these so-called<br />

heat-stable antibody opsonins are the heat-labile products of<br />

complement activation such as C3b or C3bi that are linked<br />

to particles by transacylation with the C3 thiolester. C3b<br />

combines with complement receptor 1 and C3bi combines<br />

with complement receptor 3 on phagocytic cells. Besides<br />

immunoglobulins of the mentioned isotypes and complement<br />

proteins, other opsonic complement intermediates<br />

include iC3b and C4b. Opsonins facilitate phagocytosis of<br />

particulate antigens by neutrophils or macrophages. Other<br />

substances that act as opsonins include the basement membrane<br />

constituent known as fibronectin.<br />

Inefficient phagocytosis<br />

Opsonization<br />

Fc receptor<br />

Macrophage<br />

Efficient phagocytosis<br />

Opsonization.<br />

Bacteria<br />

Antibacterial<br />

Ab (opsonin)<br />

opsonization<br />

Facilitation of the phagocytosis of microorganisms or<br />

other particles such as erythrocytes through the coating of<br />

their surfaces with immune or nonimmune opsonins. The<br />

enhanced phagocytosis of a pathogenic microorganism or<br />

macromolecule is attributable to the linkage of molecules that<br />

interact with phagocyte cell surface receptors. Antibodies<br />

such as immunoglobulin G (IgG) molecules and complement<br />

fragments may opsonize extracellular bacteria or other<br />

microorganisms, rendering them susceptible to destruction<br />

by neutrophils and macrophages through phagocytosis.<br />

opsonophagocytosis<br />

Antibodies and/or complement, mainly C3, serve as<br />

opsonins by binding to epitopes on microorganisms and<br />

increasing their susceptibility to phagocytosis by polymorphonuclear<br />

leukocytes, especially neutrophils. Serum<br />

bactericidal activity and phagocytic killing are two principal<br />

mechanisms in host defense against bacteria. Opsonic<br />

antimicrobial antibodies are critical for optimal functioning<br />

of phagocytes in the uptake and containment of bacteria.<br />

oral immunology<br />

Saliva rinses the oral cavity and also contains numerous<br />

molecules such as lysozyme and secretory immunoglobulin<br />

A (IgA) that serve as parts of the mucosal immune system to<br />

help protect the oral cavity. Polymorphonuclear leukocytes<br />

are important in protection of gingival tissues and ultimately<br />

the periodontium. In addition to secretory IgA, the systemic<br />

vascular humoral immune response is significant in oral<br />

immunity. The relative contribution of Th1 and Th2 cells<br />

in an immune response to plaque bacterial pathogens is

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