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Biotech / Medical : Indications -- Lupus/Nephritis -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (20)	4/24/2001 3:18:33 PM
From: keokalani'nui	Read Replies (1) \| Respond to of 95

: Ann Rheum Dis 2001 May;60(5):523-6 Related Articles, Books, LinkOut Expression of costimulatory molecules on peripheral blood lymphocytes of patients with systemic lupus erythematosus. Bijl M, Horst G, Limburg PC, Kallenberg CG. Department of Clinical Immunology, University Hospital, Groningen, The Netherlands. OBJECTIVE: In systemic lupus erythematosus (SLE) autoantibody production is T cell dependent. For a proper T and B cell interaction, signalling of costimulatory molecules on these cells is necessary. The expression of costimulatory molecules on peripheral blood lymphocytes in patients with SLE in conjunction with disease activity was measured to evaluate whether expression of costimulatory molecules in SLE is increased. METHODS: Thirteen patients with SLE with active disease, 10 patients with inactive disease, and 14 controls entered the study. In addition, samples from 10 of the 13 patients with active disease could be studied at a moment of inactive disease as well. Isolated peripheral blood lymphocytes were stained for the lymphocyte subset markers CD4, CD8, CD19, their respective activation markers CD25, HLA-DR, CD38, and the costimulatory molecules CD40L, CD28, CD40, CD80, and CD86. Expression was measured by flow cytometry. RESULTS: Peripheral blood lymphocytes of patients with SLE showed signs of increased activation at the moment of active disease. Almost all CD4+ T cells expressed CD28, both in patients and in controls. CD80 expression on CD19+ B cells was low in both groups and did not correlate with disease activity. In contrast, the percentage of CD19+ B cells expressing CD86 was increased in patients with SLE even in patients with inactive disease (p=0.04) and correlated with the SLEDAI score (p=0.0005) and levels of anti-dsDNA (p=0.006). No changes in CD40 or CD40L expression were found in the patients with SLE. CONCLUSION: In patients with SLE the expression of CD86 on CD19+ B cells is increased and is associated with disease activity, B cell activation, and levels of anti-dsDNA. The increased CD86 expression will render (autoreactive) B cells more susceptible for T cells. This can facilitate autoantibody production and might be a target for immunosuppressive treatments.

To: scaram(o)uche who wrote (20)	4/24/2001 3:49:03 PM
From: keokalani'nui	Read Replies (1) \| Respond to of 95

Rick. There is much in your message to gnaw on. Thank you. I've been in and out of T/TIF on more than one occaision, but it makes me feel kinda d-u-m-b. But in a good way. <g> A confession about my passion. My interest here is to understand more about this therapeutic opportunity, especially (selfishly) as it relates to 5g1.1. With membraneous nephritis the next, or second (after aMI), alxn data set, I want to understand the explanation of endpoints when it comes (though I think it is only proteinurea and complement measurements) and the competitive landscape. Why not a collaborative experiment on SI? (Little qualifier) so far, (big qualifier) to me, CLAa-Ig looks like the class of the field. Spin it may be, but ljpc has put a pretty good one on what looked like a train wreck not long ago. Finding a lot of p < .05 after buying a Biacore and re-dredging the data. I do have some instincts--the way ljpc couches their 10K business plan in terms of a drug platform makes me hold my nose. >>I'm not saying that this subset of patients won't benefit from therapy.<< Company says 90% of its PII and PII/III patients are the subset. Haven't looked into whether that would be representative of the population. Don't even know what dsDNA is! As always, thanks for the pointers. Wilder