Tcell Responses

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to obtain a specific immune response, the l-cell must interact vvilli the antigen-presenting cell <AP( ). Ibis is a complex process requiring that the I-ccll recognize the antigen on the APC, receive costimulation, activate growth cytokine receptors, and produce cytokines, which signal and support growth and differentiation. Once activated, the T-cell undergoes proliferation and differentiation, leading to one of several possible mature l-cell phenoty pes

T-cell antigen recognition is a function ol the l-cell antigen receptor, a low-affinity receptor of the immunoglobulin supertamily. I cells may express {000 to 50,000 ICRs on their surface. Antigens are presented to the K R by VtIK Class I or II molecules 011 the APC. CP I is .i related antigen-presenting molecule that presents specific antigens to NKT-cells, a unique subpopula-tion of CD4- and CPS- t-cells the l< li recognizes and binds the MTU -peptide complex.'* Antigen (Ag) is contacted by the TCR using variable domains found at the N-terminus ot the U R ot and ft subunits. f( R-peptide binding is more specific than that of the Mill -peptide, which is based on recognition of a smaller number of discontinuous amino acids. I bus the l-cell may recognize fewer antigens than those presented by the MIK

The T< R consists of a number «>1 components in addition to those that bind antigen, these include components that form the (1)3 transdnctory apparatus (TCR-CP3), which is important in the activation of the l( R and the eventual transmission or transduction «if the signal into the cell. CD8 and C 1)4 are l-cell core-ceptors whose recognition ol \IIU ( kiss I and II molecules, respectively, on APC is essential for T-cell function and subsequent It R activation, \ctivation of these corc-ceptors I) increases the excitability of the ICR and 2) increases the binding between the T-cell and the antigen-presenting cell.

I'lie low affinity of the I t R enables the l-cell to bind antigen presenting cells in a reversible manner, which occurs between multiple l( Rs and one or a few antigens over time. Ibis time-dependent interaction of many K Rs with a few antigens is referred to .is scanning. Scanning that leads to l-cell activation is called serial trixKerinx. To fully activate "I cells, multiple l< R en gagement must be sustained for 2 to 20 hours.

Activation of T-cells leads to proliferative differentiation. This process begins with activation of the protein tyrosine kinases Ick, tvn and ZAP, which activate the I ( R, phospholipase <' (PLC 1. and < 1)28 respectively d ig. 7-9). Activation of Cl>28 prepares the l-cell to receive the co-stimulatory signals, which are important in T-cell survival and function. Activation of phospholipase (

Melanosis Gingival

Color Fi(j. I 1 Left, Clinically normal gingiva in a young adult. Right, Heavily pigmented (melanotic) gingiva in a middle-aged adult (from Glickman I, Smulow |R Periodontal Disease: Clinical, Radiographic, and Histopathologic Features. Philadelphia, Saunders, 1974.)

Heavy Plaque Disclose

Color Fig. 6 1 A, Disclosed supragingival plaque covering one half to two thirds ot the clinical crowns B, Same patient as in A. Supraginqi val plaque disclosed with an oxidation-reduction dye that indicates reduced (anaerobic) areas of plaque The supragingival anaerobic areas (purple stain) are located interproximal^ and along the gingival margin C, Materia alba generalized throughout the mouth, with heaviest accumulation near the gingiva. Note the gingiva present D, Teeth stained by several weeks of mouthrinses will» alexidine. This stain can be easily removed, t, Supragingival calculus in a patient with gingival inflammation. F, Green slain on anterior teeth. Note the inflamed, enlarged interdental papilla between the maxillary central incisors (A and B, courtesy Dr. S. Soc ransky, Boston, Mass.)

Radiograph Inflamed Maxillary

Color Fig. 8 1 Periodontal manifestations of disorders affecting neutrophil function A and B, Clinical appearance of patients with cyclic neutropenia, a condition that involves reduction in the number of circulating neutrophils (blood neutrophil levels 1 SOO/rnm'). A, S-year-old boy with cyclic neutropenia. Note the aggressive and extensive inflammation in the gingival tissues. B, A 7-year-old boy with cyclic neutropenia demonstrating acute and extensive gingival inflammation and advanced attachment loss with recession evident. C and D, Clinical and radiographic appearances of patients with leukocyte adhesion deficiency (LAD type 1). This disorder involves defects in neutrophil transendothelial migration, resulting in a lack of extravascular neutrophils in periodontal lesions. However, dense infiltrates of mononuclear leukocytes are found in the periodontal lesions.170 Note the tissue inflammation evident clinically (C) and the extensive bone loss seen in these patients (D, arrows). For additional information, see text and Table 8-S. (Courtesy Dr. Max Lislgarten fA and BJ and Dr. D. C. Anderson |C and D|).

Anderson Activator Ortho AppliancePapillon Lef Vre Syndrome

Color Fig 10-1 Oral (A), radiographic (B), and dermatologic (C and D) findings in the Papillon-Lefevre syndrome (PLS). Pocketing and bone loss usually affects the primary and secondary teeth shortly after eruption. Although numerous palmoplanar keratoder-mas have been described, the hyperkeratotic lesions ol PLS can a! feet the elbows (C) and knees and the palms and plantar surfaces of the feet (D). (Courtesy Dr Robert ) Gorlin.)

Lad And Leukocytes

Color Pig. 10 2 Oral (A) and radiographic (B) appearance of a patient with leukocyte adhesion deficiency (LAD). The child was deficient in CD18 (i.e., IAD type I), which results in absent or severely reduced levels of the fi-2 integrin molecule. The patient suffered from recurrent infections of the middle ear, tongue, and perirectal areas as well as the periodontium. (From Majorana A, Notarangelo LD, Savoldi E, et al: Leukocyte adhesion deficiency in a child with severe oral irvolvement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87:691.)

Periodontal Disease Year Old Woman

Color Pig. 10-5 Reared-apart twin pairs A, 37-year-old female identical twins. Note the similarity in tooth and arch forms in the twins B. 40-year-old male fraternal twins. (From Pihlstrom B, Michalowicz B: Genetic risk for periodontal disease: A clinical perspective, journal de Paradontologie d'lmplantologie Orale 1998; 1 7:123.)

Genetics Periodontal

Color Ficj 10 4 Reared-together twin pairs A, 70-year-old male identical twins. B, 67-year-old male Iraternal twins. (From Pihlstrom B, Michalowic/ B: Genetic risk lor periodontal disease: A clinical perspective, journal de Paradontologie d'lmplantologie Orale 1998; 1 7:123.)

Supragingival Calculus Images

Color Fig 111 A, Supragingival calculus is depicted on the buccal surfaces of maxillary molars adjacent to orifice for Stenson's duct. B and C, Extensive supragingival calculus is present on the lingual surfaces of lower anterior teeth. D, Dark pigmented deposits of subgingival calculus are shown on the distal root of an extracted lower molar. Continued

Subgingival Calculus

Color Fig. Ill cont'd E, A 31 -year-old Caucasian man is shown with extensive supragingival and subgingival calculus deposits throughout his dentition. F, The same patient as shown in E, 1 year after receiving thorough scaling and root planing to remove supragingival and subgingival calculus deposits followed by restorative care. Note the substantial reduction in gingival inflammation G, tobacco stains on the apical third ol the clinical crown due to cigarette smoking. H, Inflamed marginal and papillary gingiva adjacent to an overcontoured porce Iain-fused to metal crown on the maxillary left central. I, Inflamed palatal gingiva associated with a maxillary provisional acrylu partial den ture. Note the substantial difference in color of the inflamed gingiva adjacent to the premolars and lirst molar compared with the gingiva adjacent to the second molar. J, A lower incisor depicting a prominent root without any attached gingiva and accompanying gingival recession K, The same patient as shown in ), following the placement of a soft tissue gralt to gam attached gingiva and treat the gingival recession. L, Anterior open bite with flared incisors as observed n association with a habit of tongue thrusting

Gingival Inflammation Crown

F.:.] I I A A, Gingival inflammation and enlargement associated with orthodontic appliance and poor oral hygiene B, Maxillary central incisors in whit h an clastic ligature was used to close a midline diastema. Note inflamed gingival and deep probing depths C, The same patient as shown in B. A full-thickness mucoperiosteal flap has been reflected to expose the elastic ligature and angular intrabony defects around the central incisors. D, Palatal (lap reflected to reveal bony dehiscence on the maxillary lateral incisor shown in Fig. 11-30. E, A maxillary canine that illustrates gingival recession due to self-inflicted trauma by the patient's fingernail. F, The overzealous use of a toothbrush may denude the gingival epithelial surface, leaving the underlying connective tissue exposed as a painful ulcer. C, Gingival recession and hyperkeratosis of the vestibular mucosa have developed as a consequence of using chewing tobacco H, Heavy calculus deposits on facial surfaces of the upper first molar and second premolar. Note the severe gingival inflammation in the entire quadrant.

Continued

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Responses

  • hilda
    What is difference between plaque and material Alba?
    8 years ago
  • Tewelde
    What is the clinical appearance of a normal gingiva?
    8 years ago

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