Therapy of Autoimmune Diseases with Antibody to Immune Response Gene Products or to T-Cell Surface Markers

1986 ◽  
Vol 475 (1 Autoimmunity) ◽  
pp. 274-284 ◽  
Author(s):  
LAWRENCE STEINMAN ◽  
MATTHEW K. WALDOR ◽  
SCOTT S. ZAMVIL ◽  
MAE LIM ◽  
LEANORE HERZENBERG ◽  
...  
1984 ◽  
Vol 5 (3) ◽  
pp. 43-45
Author(s):  
Lawrence Steinman ◽  
Subramaniam Sriram ◽  
Matthew K. Waldor

2004 ◽  
Vol 11 (4) ◽  
pp. 686-690 ◽  
Author(s):  
Sarah L. Young ◽  
Mary A. Simon ◽  
Margaret A. Baird ◽  
Gerald W. Tannock ◽  
Rodrigo Bibiloni ◽  
...  

ABSTRACT The gut microbiota may be important in the postnatal development of the immune system and hence may influence the prevalence of atopic diseases. Bifidobacteria are the most numerous bacteria in the guts of infants, and the presence or absence of certain species could be important in determining the geographic incidence of atopic diseases. We compared the fecal populations of bifidobacteria from children aged 25 to 35 days in Ghana (which has a low prevalence of atopy), New Zealand, and the United Kingdom (high-prevalence countries). Natal origin influenced the detection of bifidobacterial species in that fecal samples from Ghana almost all contained Bifidobacterium infantis whereas those of the other children did not. Choosing species on the basis of our bacteriological results, we tested bifidobacterial preparations for their effects on cell surface markers and cytokine production by dendritic cells harvested from cord blood. Species-specific effects on the expression of the dendritic-cell activation marker CD83 and the production of interleukin-10 (IL-10) were observed. Whereas CD83 expression was increased and IL-10 production was induced by Bifidobacterium bifidum, Bifidobacterium longum, and Bifidobacterium pseudocatenulatum, B. infantis failed to produce these effects. We concluded that B. infantis does not trigger the activation of dendritic cells to the degree necessary to initiate an immune response but that B. bifidum, B. longum, and B. pseudocatenulatum induce a Th2-driven immune response. A hypothesis is presented to link our observations to the prevalence of atopic diseases in different countries.


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