The ability of H-2 antisera and their constituent K and Ia antibodies to enhance the survival of skin allografts was investigated. Ia sera were prepared from H-2 alloantisera by exhaustive absorption with donor-strain RBC and the absorbed K antibodies were also recovered by acid elution of the RBC. The removal of conventional K/D antibody in no way diminished the activity of enhancing sera over wide dose ranges in two different incompatibility systems. The recovered K/D antibodies in the doses used had at best a trivial enhancing effect. The dominant role of Ia antibodies in enhancement was confirmed by showing significant prolongation of graft survival in third-party systems where the sera covered only some of the Ia antigens in incompatibilities involving K,D and Ia differences and in homologous systems using Ia sera fractionated into their constituent mono-specificities. It is concluded that enhancement is a function of antibodies directed against Ia antigens (I region products) and that antibody against conventional histocompatibility antigens such as H-2.K, D, and by homology HL-A and Ag-B has only a minor role in passive enhancement.
Passive enhancement of H-2 incompatible skin allografts was studied in systems where the enhancing serum covered only a restricted number of Ia specificities involved in the incompatibility. Sera reacting with products of the I-A legion were effective at prolonging survival, probably to the same extent as a serum covering all the specificities of the incompatibility. Such sera also inhibited MLR in the same strain combinations. Interpretation of these and other data suggests that products of the I-B, I-E and I-C regions play a subordinate role as target antigens for enhancement. It is concluded that eider Ia antigens of different regions have different biological activities or enhancement is a function only of antibodies directed against antigens that stimulate in MLR. * This serum may also react with another, as yet unassigned, Ia specificity of the I-A or I-B region present in H-2f, H-2" and H-2b (J. R. Archer, personal communication).
Summary.-The sera of 80 newly diagnosed lung-cancer patients have been examined for immune complexes and autoantibodies. Control subjects consisted of 20 bronchitic patients and 150 normal blood donors. Immune-complex measurements used 4 established and sensitive techniques (Raji cell assay, fluid and solid-phase Clq assays and conglutinin-binding assay) and a 5th newly devised technique based on the binding of polyethylene-glycol-precipitated immune-complex-rich serum fractions to Staphylococcus aureus. Using the Raji cell assay and the S. aureus binding assay to measure immune complexes, both newly diagnosed lung cancer patients and bronchitic patients had significantly higher prevalences of immune complexes than normal controls, but the two groups of patients did not differ significantlv in either prevalence or quantity of immune complexes. When techniques which depend solely upon complement fixation (Clq assays and conglutinin binding) were used, only meagre quantities of immune complexes were found, and in at most 15% of newly diagnosed lung-cancer patients. The presence of autoantibodies in newly diagnosed cancer patients and controls appeared to correlate with the increase in the detectable prevalence of immune complexes.
The adult kidney replaces its parenchyma in vivo in steady state and during regeneration by segment-specific clonal cell proliferation.To understand human adult kidney clonal cell growth, we derived tissue from human nephrectomies and performed limiting dilution to establish genuine clonal cultures from one single cell.Clonal efficiency of the human kidney was x%. Remarkably, a single renal cell could give rise to up to 3.3*10(6) cells. Phenotypically, two types of clonal cultures were apparent; a stably proliferating cuboidal epithelial-like appearing (EL) and a rapidly proliferating fibroblast-like appearing (FL). RNA sequencing of all clonal cultures separated FL from EL cultures according to proximal-distal/collecting renal epithelial tubular identity, respectively. Moreover, distinct molecular features in respect to cellcycle, epithelial-mesenchymal transition, oxidative phosphorylation, BMP signaling pathway and cell surface markers were observed for each clone type. Surprisingly, clonal expansion (>3 months) was sustained in EL clones harboring markers of mature kidney epithelia (high CD24, CDH1, EpCAM, EMA) in contrast to dedifferentiated FL clones (high NCAM1, serpine1), which showed fast lineage amplification and exhausted in a few weeks. Thus, the human adult kidney harbors progenitor cell function in which segment identity and the level of epithelial differentiation dictate clonal characteristics.2 4 . Liu, J., et al., Loss of SETD2 Induces a Metabolic Switch in Renal Cell Carcinoma Cell Lines toward Enhanced Oxidative Phosphorylation . J Proteome Res, 2019. 18(1): p. 331-340.2 5 . , L., et al., Clear Cell Renal Cell Carcinoma is linked to Epithelial-to-Mesenchymal Transition and to Fibrosis. Physiol Rep, 2017. 5(11.( 2 6 . Sanchez, D.J. and M.C. Simon, Genetic and metabolic hallmarks of clear cell renal cell carcinoma. Biochim Biophys Acta Rev Cancer, 2018. 1870(1): p. 23-31. Landolt2 7 .Buzhor, E., et al., Cell-based therapy approaches: the hope for incurable diseases. Regen Med, 2014. 9(5): p. 649-72. 2 8 . Chuang, C.H., et al., Molecular definition of a metastatic lung cancer state reveals a targetable CD109-Janus kinase-Stat axis. Nat Med, 2017. 23(3): p. 291-300.
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