MHC restricted and non-restricted killer lymphocytes

This study investigated the prognostic performance of the systemic immune-inflammation index (SII) in patients with epithelial ovarian cancer (EOC) in Lagos, Nigeria.We performed a secondary analysis of the data of 91 women who had treatment for EOC between 2009 and 2018. The associations between pretreatment SII and survivals were tested.Pretreatment SII more than 610.2 was a significant independent predictor of reduced progression-free survival (HR = 2.68; 95% CI, 1.17 to 6.09) while SII greater than 649.0 was a significant independent predictor of reduced 3-year overall survival (HR = 2.01; 95% CI, 1.01 to 3.99).These findings suggest that high SII may be a potential prognostic indicator and useful marker for more intensive surveillance and design of personalized treatment in patients with EOC.This study looked at how the systemic immune-inflammation index (SII) can predict the outcomes of patients with epithelial ovarian cancer (EOC). To do this, the data of 91 women who received treatment for EOC between 2009 and 2018 were analyzed. The study concluded that when the SII level was higher than 610.2 and 649.0, it was linked to a higher likelihood of EOC progressing sooner and of reduced survival at the 3-year mark, respectively. This suggests that a high SII might be a useful predictor to understand how EOC could progress and how well patients with EOC might survive. 

Prognostic performance of pretreatment systemic immune-inflammation index in women with epithelial ovarian cancer

Murine spleen cells activated by concanavalin A (Con A) in culture produce a class of lymphokine molecules which possess biological activity in a number of lymphocyte response assays. Lymphokines with a mol wt of 30,000, as estimated from gel filtration studies, can be resolved into two components which differ by charge, with isoelectric point (pI) values of 4.3 and 4.9, respectively. Both components stimulate (a) the growth of established T-cell lines in culture, (b) the proliferation of thymocytes in the presence of Con A under culture conditions where Con A alone is nonmitogenic, (c) the induction of antibody responses to heterologous erythrocyte antigens in athymic (nude) spleen cultures, (d) the generation of cytotoxic T lymphocytes (CTL) in thymocyte cultures, and (e) the generation of CTL in nude spleen cultures. In each of these culture systems we suggest that the assays are detecting a single class of lymphokine which acts directly on activated T cells. Nonactivated T cells must be stimulated by either antigen or mitogen before becoming responsive to lymphokine, but do not require antigen or mitogen for continued growth with lymphokine. The two molecular species, separable by isoelectric focusing are referred to as the T-cell growth factor (TCGF). A lymphokine, similar in size (30,000 daltons) to TCGF but heterogeneous in charge (pI 3.0--4.0), stimulates immune responses to erythrocyte antigens in T-cell-depleted spleen cultures but has no stimulatory activity in the other lymphocyte assay systems described. The data have been interpreted as showing the two molecular forms of murine TCGF (pI 4.3 and 4.9) are responsible for many of the lymphokine activities described elsewhere as thymocyte mitogenic factor, nonspecific T-cell-replacing factor and killer helper factor or costimulator. The other lymphokine, separable from TCGF by charge, appears to have true T-cell-replacing activity.

Regulatory molecules. I. Purification of a class of murine lymphokines.

Accumulating evidence indicates that the central nervous system (CNS) may regulate the activity of the immune system. Although the overall significance of the immune system in cancer remains controversial, psychosocial influences on immune function could potentially provide a mechanism to account for some of the reports of an association between psychosocial factors and cancer prognosis.

Psychoneuroimmunology. Implications for oncology

Despite the considerable achievements in immunology during the past two decades, control of tumour development by effective immunotherapy is still not possible. This situation reflects the complexity of events that occur in response to tumour growth. Other chapters in this book outline the important advances made in the study of macrophage function and the developments in monoclonal antibody production against tumour-associated antigens. In this chapter the role of the lymphocyte in combating tumour development and metastatic spread is considered. Of importance, however, is the understanding that lymphocyte function is influenced by other cell types, hormones, and products released by tumour cells and that much of our current knowledge has stemmed from in vitro experimentation. Caution must be exercised when interpreting the results of laboratory tests and relating these to their in vivo relevance, since it is not possible to mimic the conditions that the in vivo environment imposes on lymphocyte activity.

Antitumour Lymphocyte Responses

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Antitumour Lymphocyte Responses