DleI pt et s oI.eS f Pathologv and o -'eriodollicis, and Cel terf' for Researchl i Oral I.,log .,UfIieri l o.fI IX \\,'t.fI1,inI"toll School of5Mediif , Seattle, Washinigton 9S/9-5 le effect of' in/flammttillon oil leit distribution f 'collag'tzens types I, I, IV, and V and Istype' 1 i/ I trier tdilnonecutiln ilihuman 14,i/gilvat w'.as studied s (/er staining 1th1('m withl anti bodies to these )rotein.s. Ginltival antibodies, and l staining was visualized by ifndirct itmmiune fluor estcene using FITCi or rholidam itne-conj 'tuated second antibodlies. The resullls sholi edthat at/ihodtl o typ Ie I oltlagtl sta in/td /tomaluini ', al/ 'oneti l' ti.sstl unitrmly and revealed thelt presence of thick fi.bert bundles. The fstaitning wis, xpart'se at arIas of( it /flat matit and lcukoc(\tic it/nfilt-ration. Alti-t\pe-II anbtibodv rtevealed a finefi'brillatr network in the normal ginfgiva, especially near the epithelium:l Ihe tyNpe I also lost ss o ls 1it of1fla atio. Type V c1ollag9ln atttibvody 1alo stained the tins ilu(one('ti'C tissue intensely bul. unlike the ftresI and III staining, it was retained inflamed areas. Normal iniage hl'iWernotl(t Stlilted b tlie b pe I tit an1 t1t ei tbodv, hot\'h'er, suptpaini e o('(urred at irelamsedrsiies. Both nornftl andiI inflamed tissues wert'e stained bv t\'pe IV 'collatg^en a(1ibodv, andthe staining 'was restrictlled to basement me fbranesltaruc urs. The o11lalaeltd inflaliled gingiv'ae containedd a tyhi'cfilr network which bound antifibroenectin antibody. We conclude that the various gingival cllagen fillers are made tq) of collagen types I, III, and V, that the types I and II collagens are perentially lost during inflam nation, and that type I triner appears at inflame ed sites.

Gingivitis and periodontitis account for more than 95% of all inflammatory diseases of the tissues surrounding the teeth, comprising the principal cause of tooth loss in adults. Gingivitis is a relatively innocuous inflammation of the gums, with associated bleeding and exudation. Gingivitis may convert to periodontitis, a destructive aggressive disease with resorption of alveolar bone, destruction of collagen with fibrosis, and formation of deep pockets around the necks of the teeth. Gingivitis and periodontitis are caused by microorganisms populating the gingival sulcus and periodontal pocket. Treatment is directed toward arresting the progress of the disease through debridement and stabilization of the teeth. Toothbrushing and other measures by which the teeth are mechanically cleaned remain the most effective way to control plaque accumulation and periodontal disease.

The extensive breakdown of immune homeostasis in the motheaten mouse (me/me) has been ascribed to a single gene defect on chromosome 6 (ref. 1). These mice develop skin lesions within the first week of life, do not thrive, and die within the first 3--8 weeks. There is severe hypergammaglobulinaemia with multiple species of circulating autoantibody and deposition of immune complexes in the thymus, skin, lungs and kidneys. A single gene defect producing such catastrophic results may provide an important model for understanding autoimmune phenomena. We report here a virtual absence of terminal deoxynucleotidyl transferase-positive (TdT+) cells in the bone marrow, thymus and spleen of motheaten mice. TdT is a DNA polymerase which has the unique capacity to polymerize nucleotides in the absence of template direction. Although no in vivo biological function of this enzyme has been established, its unique appearance in the bone marrow and thymus of adult mammals and its in vitro biochemical activity have led to a proposed role for TdT in the somatic diversification of lymphocytes. Bone marrow TdT+ cells have been shown to belong to both T and B cell populations and may also include precursor cells common to these lineages. Although the role of TdT in the acquisition of appropriate T- and B-cell specificities is not known, our results are the first to correlate the virtual absence of TdT+ cells with a severe autoimmune syndrome. We investigated the level of TdT+ cells in neonatal me/me mice and their normal littermates and the susceptibility of TdT+ cells to circulating autoantibody in motheaten mouse serum.

No abstract

That a central immunological unresponsive state exists to our own body constituents is widely accepted. The precise role played by the various cell types of the lymphoid system in the maintenance or abrogation of this unresponsiveness to self remains unclear. A large number of nonself-antigens require the collaboration of thymus-derived (T) and bone marrow-derived (B) lymphocytes (1, 2). Although both T and B cells may be made unresponsive, only one cell type need be in order that the intact animal remain unresponsive (3). In a rabbit model, the cellular events in the termination of unresponsiveness to bovine serum albumin (BSA), 1 by the injection of cross-reacting albumins, were best explained by assuming that the T cells, but not the B cells, were unresponsive to BSA and to cross-reacting determinants on other albumins (4). Such a situation may explain the apparent ease with which unresponsiveness to self components may be abrogated in autoimmune disorders such as thyroiditis (5-7) and rheumatic fever (8).The present investigations were undertaken to directly assess by adoptive transfer, antigen-binding and antigen-suicide techniques, the interactions of T and B cells during the induction of autoantibody to syngeneic thyroglobulin (Tg) and during the production of thyroid lesions. Materials and Methods Immunization of Mice with HeterologousTg.--6--8-wk old female A/J mice (Jackson Laboratories, Bar Harbor, Maine) were injected intraperitoneally with 0.5 mg of an equal mixture * Publication no. 788 from