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The spectrum of salivary gland function in primary Sjogren's syndrome
Abstracts
599
THE SPECTRUM OF SALIVARY GLAND FUNCTION IN PRIMARY SJOGREN'S SYNDROME. Jane C. Atkinson, Alice A. Macynski and Philip C. Fox. CIPCB,NIDR,NIH, -R&he<&. Mll IEA ___.,____,.._-.. The major salivary gland function of 63 individuals with primary Sjogren's syndrome was studied. All had labial minor salifary gland biopsies demonstrating at least a single focal lymphocytic infiltrate/4 nzn of tissue. Each subject had unstimulated and stimulated saliva collected from individual parotid and submandibular glands in a standardized manner between 9 and 11 am. Stimulation was obtained by repeated application of 2% citrate to the anterior dorsal tongue surface at 30 set intervals. Flow rate was calculated and expressed as ml/min/gland. All subjects complained of oral dryness (xerostomia) and most had additional complaints of difficulty swallowing, eating and speaking. Only 3 individuals (5%) had measurable unstimulated parotid output, although 27 (43%) had stimulated flow above the minimally normal level of 0.05 ml/min/gland. For the group, the mean stimulated parotid output (+SEM) was 0.086 (tO.02) ml/min/gland. In contrast, while 6 subjects had some unstimulated submandibular flow, only 7 of the 63 (11%) had stimulated output above minimally normal levels (0.05 ml/min/gland). The mean stimulated submandibular output was 0.036 (kO.02) ml/min/gland. The median value was 0 for this collection group and for stimulated parotid flow was 0.016 ml/min/gland. There was no significant correlation found between stimulated parotid output and minor salivary gland biopsy scores in a subset of 19 patients. These results demonstrate that the group, as a whole, had severe salivary gland dysfunction. Additionally, it was shown that submandibular function was more severely affected than parotid output and that These results suggest that stimulated parotid function was most preserved. measurement of only stimulated parotid gland salivary output, while convenient, is not truly reflective of major salivary gland function or minor gland inflammatory changes.
CD4'
SUBSETS IN SJOGREN'S SYNDROME.
- PA Bacon,
GD Kitas, M Salmon,
J Mathews, J Hamburger and J Potts,
University of Biimiogbam, Birmingham, UK. Sjogrcn’s Syndrome (SS) is charactcriscd by chronic ictlammation of the exocrine glands. A marked lymphoid infiltrate is found at the inflammatory sites, with a predominance of CD4 + helper T cells, a picture reflected also in the peripheral blood. Several disturbances of immunoregulation have been demonstrated in SS, both in viva and in vitro, including reduced delayed type hypersensitivity responses to recall antigens, impaired proliferation of lymphocytes to mitogcns, depressed natural killer cell activity and diminished autologous mixed lymphocyte reaction. Most of these defects may be at least partially explained by a deficiency of Interleukio-2 (lL2) production, which has also been shown to occur in SS. CD4 + T cells, the major IL2 producing populatloo, have recently been shown to comprise of hvo founctionallyand phenotypieally distinct subsets: The CD4 + 2H4 + (suppressor-inducers) and CD4 + 2H4-4B4 + (helper-inducers). We have recently shown that of these subsets, only the CD4+2H4+
produce ILZ. A specitic loss of this subset has been shown
to occur in active SLE and RA and may partially explain the deficient IL-2 production observed in these diseases. We are currently investigating the distribution of the CD4 + subpopulations in the peripheral blood, minor salivary glands and other inflammatory sites of patients with primary and secondary SS, as a means to further understand the defective immunoregulation io this disease.
IDENTIFICATION OF AN AUTOEPITOPE ON RO/SSA. WD Dickey, KW Jackson, MK Sanner, SL Delltscher, JD Keene, and JB Harley, Arthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma University Health Sciences Center and Veterans Administration Medical Center, Oklahoma City, OK, and Department of Microbiology, Duke University, Durham, NC (USA) The 60 kd RoiSSA autoantigen was purified by ion exchange, affinity, and gel filtration chromatography to apparent homogeneity as judged by SDS polyacrylamide gel elcctrophoresis. The purified bovine antigen was partially digested with Staphylococcal V-E protease employing mild denaturing conditions and the resulting peptides evaluated using immunoblotting techniques. Serum from rabbits immunized with purified bovine Ro/SSA identified multiple peptides with apparent molecular weights of 50 kd to I1 kd while human autoimmune sera bound to only a few. The smallest prptide
identified
that
retained
antigenicity
had
an
estimated
molecular
weight
of
599
THE SPECTRUM OF SALIVARY GLAND FUNCTION IN PRIMARY SJOGREN'S SYNDROME. Jane C. Atkinson, Alice A. Macynski and Philip C. Fox. CIPCB,NIDR,NIH, -R&he<&. Mll IEA ___.,____,.._-.. The major salivary gland function of 63 individuals with primary Sjogren's syndrome was studied. All had labial minor salifary gland biopsies demonstrating at least a single focal lymphocytic infiltrate/4 nzn of tissue. Each subject had unstimulated and stimulated saliva collected from individual parotid and submandibular glands in a standardized manner between 9 and 11 am. Stimulation was obtained by repeated application of 2% citrate to the anterior dorsal tongue surface at 30 set intervals. Flow rate was calculated and expressed as ml/min/gland. All subjects complained of oral dryness (xerostomia) and most had additional complaints of difficulty swallowing, eating and speaking. Only 3 individuals (5%) had measurable unstimulated parotid output, although 27 (43%) had stimulated flow above the minimally normal level of 0.05 ml/min/gland. For the group, the mean stimulated parotid output (+SEM) was 0.086 (tO.02) ml/min/gland. In contrast, while 6 subjects had some unstimulated submandibular flow, only 7 of the 63 (11%) had stimulated output above minimally normal levels (0.05 ml/min/gland). The mean stimulated submandibular output was 0.036 (kO.02) ml/min/gland. The median value was 0 for this collection group and for stimulated parotid flow was 0.016 ml/min/gland. There was no significant correlation found between stimulated parotid output and minor salivary gland biopsy scores in a subset of 19 patients. These results demonstrate that the group, as a whole, had severe salivary gland dysfunction. Additionally, it was shown that submandibular function was more severely affected than parotid output and that These results suggest that stimulated parotid function was most preserved. measurement of only stimulated parotid gland salivary output, while convenient, is not truly reflective of major salivary gland function or minor gland inflammatory changes.
CD4'
SUBSETS IN SJOGREN'S SYNDROME.
- PA Bacon,
GD Kitas, M Salmon,
J Mathews, J Hamburger and J Potts,
University of Biimiogbam, Birmingham, UK. Sjogrcn’s Syndrome (SS) is charactcriscd by chronic ictlammation of the exocrine glands. A marked lymphoid infiltrate is found at the inflammatory sites, with a predominance of CD4 + helper T cells, a picture reflected also in the peripheral blood. Several disturbances of immunoregulation have been demonstrated in SS, both in viva and in vitro, including reduced delayed type hypersensitivity responses to recall antigens, impaired proliferation of lymphocytes to mitogcns, depressed natural killer cell activity and diminished autologous mixed lymphocyte reaction. Most of these defects may be at least partially explained by a deficiency of Interleukio-2 (lL2) production, which has also been shown to occur in SS. CD4 + T cells, the major IL2 producing populatloo, have recently been shown to comprise of hvo founctionallyand phenotypieally distinct subsets: The CD4 + 2H4 + (suppressor-inducers) and CD4 + 2H4-4B4 + (helper-inducers). We have recently shown that of these subsets, only the CD4+2H4+
produce ILZ. A specitic loss of this subset has been shown
to occur in active SLE and RA and may partially explain the deficient IL-2 production observed in these diseases. We are currently investigating the distribution of the CD4 + subpopulations in the peripheral blood, minor salivary glands and other inflammatory sites of patients with primary and secondary SS, as a means to further understand the defective immunoregulation io this disease.
IDENTIFICATION OF AN AUTOEPITOPE ON RO/SSA. WD Dickey, KW Jackson, MK Sanner, SL Delltscher, JD Keene, and JB Harley, Arthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma University Health Sciences Center and Veterans Administration Medical Center, Oklahoma City, OK, and Department of Microbiology, Duke University, Durham, NC (USA) The 60 kd RoiSSA autoantigen was purified by ion exchange, affinity, and gel filtration chromatography to apparent homogeneity as judged by SDS polyacrylamide gel elcctrophoresis. The purified bovine antigen was partially digested with Staphylococcal V-E protease employing mild denaturing conditions and the resulting peptides evaluated using immunoblotting techniques. Serum from rabbits immunized with purified bovine Ro/SSA identified multiple peptides with apparent molecular weights of 50 kd to I1 kd while human autoimmune sera bound to only a few. The smallest prptide
identified
that
retained
antigenicity
had
an
estimated
molecular
weight
of