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Articles by K. C Barnes
Total Records ( 2 ) for K. C Barnes
  R. B Pearlman , P. R Golchet , M. G Feldmann , L. A Yannuzzi , M. J Cooney , J. E Thorne , J. C Folk , E. H Ryan , A Agarwal , K. C Barnes , K. G Becker and L. M. Jampol
 

Objective  To determine whether there is an increased prevalence of systemic autoimmune diseases in both patients with white spot syndromes (WSS) and their family members.

Methods  Patients with WSS at participating institutions were asked to complete a questionnaire reporting their own medical histories as well as any autoimmune diseases among their first- and second-degree relatives.

Results  As of January 1, 2008, 114 questionnaires had been collected, providing medical histories of 114 patients with WSS and 1098 family members. The number of patients with WSS with self-reported systemic autoimmune diseases was 26 (23%). Of 1098 relatives, 106 (10%) had at least 1 autoimmune disease. Systemic autoimmunity was more prevalent in female relatives (13%) as compared with male relatives (6%). In addition, the prevalence of autoimmunity was significantly higher among first-degree relatives (13%) than second-degree relatives (8%). Patients who themselves had systemic autoimmune diseases showed a greater prevalence of systemic autoimmunity among their families as compared with the families of patients without systemic autoimmune diseases.

Conclusions  Our data indicate that there is an increased prevalence of systemic autoimmunity in both patients with WSS and their first- and second-degree relatives. This suggests that WSS occur in families with inherited immune dysregulation that predisposes to autoimmunity.

  N. R Aggarwal , F. R D'Alessio , K Tsushima , V. K Sidhaye , C Cheadle , D. N Grigoryev , K. C Barnes and L. S. King
 

In animal models of acute lung injury (ALI), gene expression studies have focused on the acute phase of illness, with little emphasis on resolution. In this study, the acute phase of intratracheal lipopolysaccharide (IT LPS)-induced lung injury was similar in wild-type (WT) and recombinase-activating gene-1-deficient (Rag-1–/–) lymphocyte-deficient mice, but resolution was impaired and resolution-phase lung gene expression remained different from baseline only in Rag-1–/– mice. By focusing on groups of genes involved in similar biological processes (gene ontologies) pertinent to inflammation and the immune response, we identified 102 genes at days 4 and 10 after IT LPS with significantly different expression between WT and Rag-1–/– mice. After adoptive transfer of isolated CD4+CD25+Foxp3+ regulatory T cells (Tregs) to Rag-1–/– mice at the time of IT LPS, resolution was similar to that in WT mice. Of the 102 genes distinctly changed in either WT or Rag-1–/– mice from our 7 gene ontologies, 19 genes reverted from the Rag-1–/– to the WT pattern of expression after adoptive transfer of Tregs, implicating those 19 genes in Treg-mediated resolution of ALI.

 
 
 
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