|1.||Phillips, S: 1 article (10/2000)|
|2.||Sherr, A: 1 article (10/2000)|
|3.||Grossman, R: 1 article (10/2000)|
|4.||Singer, G: 1 article (10/2000)|
|5.||Gilleaudeau, P: 1 article (10/2000)|
|6.||Lebwohl, M: 1 article (10/2000)|
|7.||Shirin, S: 1 article (10/2000)|
|8.||Solodkina, G: 1 article (10/2000)|
|9.||Neisler, H M: 1 article (10/2000)|
|10.||Gisoldi, E: 1 article (10/2000)|
05/01/1994 - "CD4 (OKT4a) monoclonal antibody blocks their infection. "
05/01/1993 - "Furthermore, infection could be blocked by anti-CD4 monoclonal antibody OKT4a indicating a CD4 mediated viral entry in HEp-2 cells. "
01/01/1992 - "This anti-idiotypic antibody to OKT4A is less frequent than the antibody reacting with T4.2. In two patients studied, this OKT4A binding antibody seems to appear as early during infection as the anti-idiotypic antibody to T4.2; however, the concentration varies more with time. "
04/01/1991 - "In our experimental conditions the blocking the CD4 receptor of human monocytes with OKT4A monoclonal antibody did not prevent HIV-1 infection, although the level of virus replication appeared lower than that in cultures without OKT4A. "
01/01/1986 - "T cells of the suppressor/cytotoxic (OKT8F) phenotype predominated regardless of the infection protocol, and perifollicular T lymphocytes of both the suppressor/cytotoxic and helper (OKT4A) phenotypes appeared in large numbers during the peak inflammatory reaction. "
|2.||T-Cell Lymphoma (Lymphoma, T Cell)
|3.||HIV Infections (HIV Infection)
02/15/1987 - "Incomplete inhibition of the HTLV-III infection of a T4-positive (LDV-7) and a T4-negative (Craig) was obtained by preadsorption with specific MAb to T4 (OKT4A and Leu 3A). "
02/15/1998 - "Exposure of MKs to saturating concentration of anti-CD4 OKT4A monoclonal antibody (MoAb), which recognizes the CD4 region binding with the gp120 envelope glycoprotein, markedly inhibited HIV infection, as indicated by a reduction of p24 content in the supernatants: because the inhibitory effect was incomplete, it is apparent that the infection is only partially CD4-dependent, suggesting that an alternative mechanism of viral entry may exist. "
12/15/1990 - "The peptide CD4(23-56), derived from a region of CD4 implicated in binding of CD4 antibodies that neutralize HIV infection and cell fusion, had no effect on CD4-dependent cell fusion, HIV-1 infection, or CD4/gp120 binding, but did reverse OKT4A and anti-Leu 3a blockade of gp120 binding to CD4. "
12/01/1992 - "Furthermore, despite the absence of CD4 expression, both T cell lines were susceptible to CD4-independent HIV-1 superinfection (lack of superinfection inhibition in the presence of OKT4A monoclonal antibodies)."
07/01/1992 - "Comparative flow cytometry of L-2 and M10 cells revealed that the cell surface of L-2 cells despite expressing HIV-1 env protein, reacted slightly with OKT4 or anti-CD4(68-130) MAb, but not with Leu-3a or OKT4A MAb. In contrast, no reaction was detected with any of these anti-CD4 MAbs on the surface of another HIV-1 superinfection-resistant cell clone, MOLT-#8IIIB-14, which expresses HIV-1 env proteins but does not produce infectious HIV-1 particles. "
|5.||Psoriasis (Pustulosis Palmaris et Plantaris)
10/01/2000 - "Targeting CD4 using sequential treatments with a humanized monoclonal antibody (OKTcdr4a) may offer another therapeutic option for the treatment of moderate to severe psoriasis."
02/01/1998 - "Six patients with recalcitrant plaque psoriasis (PASI>12) received a humanized non-depleting monoclonal antibody to CD4 (ORTHOCLONE OKT(R)cdr4a). "
|4.||recombinant soluble CD4
|8.||Complementarity Determining Regions (Complementarity Determining Region)
|9.||Muromonab-CD3 (Muromonab CD3)
|10.||CD4 Antigens (CD4 Antigen)