Disease relevance of RHOJ

• We selected a panel of 721 COP-reactive T cell lines (TCL) from the blood of COP-treated and untreated multiple sclerosis patients and from healthy donors by using the split-well cloning technique [1].
• Cytotoxic T-cell lines (TCL) with specificity for host pretransplant PBMC were obtained from 9 of these patients, all presenting with severe graft-versus-host disease (GVHD), but from none of the remaining cases lacking evidence of disease [2].
• Sixty-three patients with T-cell lymphoma (TCL) were analyzed to correlate morphological and immunological features with clinical presentation, response to therapy, and survival [3].
• BALB/c Th cell lines (TCL), specific for either the Mycoplasma arthritis-derived SA or the Staphylococcus aureus-derived toxic shock syndrome toxin-1) were generated [4].
• Although it has been proposed that autoimmune disease could result from the failure of normal deletional mechanisms, this preliminary survey of MBP-reactive mature TCL from multiple sclerosis patients revealed that such cells are highly susceptible to TCR-induced PCD and comparable with TCL from normal subjects [5].

Psychiatry related information on RHOJ

• The choice of TCL/TK as development language and the adoption of well-defined software architecture were found to be the success key factors [6].

High impact information on RHOJ

• A cloned, trinitrophenyl (TNP)-specific helper T cell line (TCL), termed E-11, has been established in long-term, interleukin 2-dependent culture and used to study human T helper (Th)-B cell collaboration [7].
• E-11 helper activity is not constitutive, but requires antigen-specific, major histocompatibility complex-restricted activation of the TCL cells by interaction with TNP-modified autologous or DR 5+ allogeneic macrophages [7].
• In these patients 75-87% of the TCL responded to a single, patient-specific cluster of immunodominant T cell epitopes located within a small (20-amino acid) domain of MBP [8].
• Moreover, this TCL suppressed the specific proliferation of autologous peripheral blood lymphocytes to S. japonicum egg antigen [9].
• The majority of the COP-reactive TCL from untreated multiple sclerosis patients and normal donors predominantly produced IFN-gamma and, accordingly, were classified as T helper 1 cells (TH1) [1].

Chemical compound and disease context of RHOJ

• To our knowledge, this is the first demonstration of food allergen-specific TCL establishment and identification of a T cell epitope possibly related to the allergic reaction to food antigens [10].

Biological context of RHOJ

• This GTPase, termed as TC10-like (TCL) is encoded by an unexpectedly large locus, made of five exons spanning over 85 kilobases on human chromosome 14 [11].
• The same phenotype is generated by replacing the C terminus of dominant active Cdc42 and TC10 with that of TCL, indicating that all three proteins share downstream effector proteins [12].
• The expression pattern of some of them was similar to TCL/TC10betaL expression in adipogenesis, suggesting that the expression of these genes would be regulated by TCL/TC10betaL [13].
• Because of its capacity to enhance class I MHC antigen expression, IFN-gamma represents a key cytokine for determining the susceptibility of MiHA targets for lysis by TCL and clones, and in one patient an MiHA-specific clone recognized host leukemic cells and also inhibited host leukemic cell growth in a colony inhibition assay [2].
• Although major histocompatibility complex restriction of this T-B interaction operates at the inductive level, help is at least partially unrestricted at the effector level as alloantigen-activated TCL cells provide demonstrable, although not maximal, help for DRw1- B cells [14].

Anatomical context of RHOJ

• Thus, TCL is essential for clathrin-dependent endocytosed receptors to enter the early/sorting endosomes [12].
• These results strongly indicated that TCL/TC10betaL has a crucial role in the early stage of adipocyte differentiation, probably linked to the PPARgamma pathway [13].
• Moreover, the sense TCL/TC10betaL-expressing experiment using NIH-3T3 cells, which do not usually differentiate into adipocytes, clearly showed the accumulation of oil droplets as well as the elevated expression of various adipogenic marker genes in the presence of the ligand for peroxisome proliferator-activated receptor gamma (PPARgamma) [13].
• Whereas hematopoietic cells such as phytohemagglutinin (PHA) blasts or lymphoblastoid cell lines were susceptible to lysis by MiHA-specific TCL, keratinocytes (K) representing the natural targets of GVHD were quite resistant [2].
• We used a panel of class II-restricted T cell lines (TCL), generated against trinitrophenyl (TNP)-modified autologous peripheral blood mononuclear cells (PBMC), to examine the antigen-presenting functions of various PBMC-derived class II-positive cell types, including adherent cells, B + null cells, and activated T cells [15].

Associations of RHOJ with chemical compounds

• Stimulation of PBMC or allergen-specific TCL with either nArt v 1 or rArt v 1 resulted in comparable proliferative T cell responses [16].
• TCL with identical restriction elements and similar responses to truncated peptides could be differentiated further using alanine-substituted peptides [17].
• STAT3 displayed tyrosine phosphorylation and DNA binding in all (four of four) ALK+ TCL cell lines tested [18].
• We showed that citrulline affects antigen recognition by some TCL that are specific for areas of MBP that contain the citrulline residues [19].
• The tibial and fibular collateral ligaments (TCL and FCL) were evaluated on coronal SE images (TE = 30 ms, TR = 200 or 530 ms; TE = 120 ms, TR = 2,000 or 2,120 ms) [20].

Other interactions of RHOJ

• Conversely, in the presence of dominant active TCL, internalized Tf accumulates in early endosome antigen-1-positive early/sorting endosomes and not in perinuclear recycling endosomes [12].

Analytical, diagnostic and therapeutic context of RHOJ

• We used intracellular double-immunofluorescence flow cytometry for quantitative analysis of cytokine production (IL-4, IFN-gamma) by the TCL [1].
• Coculture of cloned alloproliferative TCL cells with a panel of allogeneic stimulators reveals that these clones are specifically reactive against the HLA-DRw1 determinant [14].
• Th1/ Th2 cytokine production by stimulated TCL (72 hours) was analyzed by enzyme-linked immunosorbent assay [21].
• Epitope mapping of TCL and TCC using overlapping peptides revealed a single immunodominant T cell epitope recognized by 81% of the patients [16].
• Of greater interest, coculture of selected alloproliferative TCL cells with DRw1+ but not DRw1- B cells results in a vigorous polyclonal response as measured by the reverse hemolytic plaque assay [14].

References