Health care organizations have increasingly acknowledged the presence of health care disparities across race/ethnicity and socioeconomic status, but significantly fewer have made health equity for diverse patients a true priority. Lack of financial incentives is a major barrier to achieving health equity. To create a business case for equity, governmental and private payors can: 1) Require health care organizations to report clinical performance data stratified by race, ethnicity, and socioeconomic status. 2) Incentivize preventive care and primary care. Implement more aggressive shared savings plans, update physician relative value unit fee schedules, and encourage partnerships across clinical and non-clinical sectors. 3) Incentivize the reduction of health disparities with equity accountability measures in payment programs. 4) Align equity accountability measures across public and private payors. 5) Assist safety-net organizations. Provide adequate Medicaid reimbursement, risk-adjust clinical performance scores for sociodemographic characteristics of patients, provide support for quality improvement efforts, and calibrate cuts to Disproportionate Share Hospital (DSH) payments to the pace of health insurance expansion. 6) Conduct demonstration projects to test payment and delivery system reform interventions to reduce disparities. Commitment to social justice is essential to achieve health equity, but insufficient without a strong business case that makes interventions financially feasible.

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<div>AbstractPurpose:<p>Immune dysregulation is described in multiple myeloma. While preclinical models suggest a role for altered T-cell immunity in disease progression, the contribution of immune dysfunction to clinical outcomes remains unclear. We aimed to characterize marrow-infiltrating T cells in newly diagnosed patients and explore associations with outcomes of first-line therapy.</p>Experimental Design:<p>We undertook detailed characterization of T cells from bone marrow (BM) samples, focusing on immune checkpoints and features of immune dysfunction, correlating with clinical features and progression-free survival.</p>Results:<p>We found that patients with multiple myeloma had greater abundance of BM regulatory T cells (Tregs) which, in turn, expressed higher levels of the activation marker CD25 compared with healthy donors. Patients with higher frequencies of Tregs had shorter PFS and a distinct Treg immune checkpoint profile (increased PD-1, LAG-3) compared with patients with lower frequencies of Tregs. Analysis of CD4 and CD8 effectors revealed that low CD4effector (CD4^eff):Treg ratio and increased frequency of PD-1–expressing CD4^eff cells were independent predictors of early relapse over and above conventional risk factors, such as genetic risk and depth of response. <i>Ex vivo</i> functional analysis and RNA sequencing revealed that CD4 and CD8 cells from patients with greater abundance of CD4^effPD-1⁺ cells displayed transcriptional and secretory features of dysfunction.</p>Conclusions:<p>BM-infiltrating T-cell subsets, specifically Tregs and PD-1–expressing CD4 effectors, negatively influence clinical outcomes in newly diagnosed patients. Pending confirmation in larger cohorts and further mechanistic work, these immune parameters may inform new risk models, and present potential targets for immunotherapeutic strategies.</p></div>