Health policy counterpublics: Enacting collective resistances to US molecular HIV surveillance and cluster detection and response programs

Health policies and the problems they constitute are deeply shaped by multiple publics. In this article we conceptualize health policy counterpublics: temporally bounded socio-political forms that aim to cultivate particular modes of conduct, generally to resist trajectories set by arms of the state. These counterpublics often emerge from existing social movements and involve varied forms of activism and advocacy. We examine a health policy counterpublic that has arisen in response to new forms of HIV public health surveillance by drawing on public documents and interview data from 2021 with 26 stakeholders who were critical of key policy developments. Since 2018, the national rollout of molecular HIV surveillance (MHS) and cluster detection and response (CDR) programs in the United States has produced sustained controversies among HIV stakeholders, including among organized networks of people living with HIV. This article focuses on how a health policy counterpublic formed around MHS/CDR and how constituents problematized the policy agenda set in motion by federal health agencies, including in relation to data ethics, the meaningful involvement of affected communities, informed consent, the digitization of health systems, and HIV criminalization. Although familiar problems in HIV policymaking, concerns about these issues have been reconfigured in response to the new sociotechnical milieu proffered by MHS/CDR, generating new critical positions aiming to remake public health. Critical attention to the scenes within which health policy controversies play out ought to consider how (counter)publics are made, how problems are constituted, and the broader social movement dynamics and activist resources drawn upon to contest and reimagine policymaking in public life

Gregg Deal's White Indian (2016): The Decolonial Possibilities of Museum Performance

Gregg Deal (Pyramid Lake Paiute) is a performance and visual artist whose work deals explicitly in decolonizing the contemporary experience of Indigenous peoples. An analysis of his performance ofWhite Indian in 2016 at the Denver Art Museum opens up the possibilities of performance as a method for museums to decolonize their spaces and curation

Multi-faceted role of LRP1 in the immune system

Graft versus host disease (GVHD) represents the major complication after allogeneic hematopoietic stem cell transplantation (Allo-SCT). GVHD-prone patients rely on GVHD prophylaxis (e.g. methotrexate) and generalized anti-GVHD medical regimen (glucocorticoids). New anti-GVHD therapy strategies are being constantly explored, however there is an urgent need to improve current treatment, since GVHD-related mortality reaches 22% within 5 years in patients with chronic GVHD. This review is an attempt to describe a very well-known receptor in lipoprotein studies – the low-density lipoprotein receptor related protein 1 (LRP1) - in a new light, as a potential therapeutic target for GVHD prevention and treatment. Our preliminary studies demonstrated that LRP1 deletion in donor murine T cells results in significantly lower GVHD-related mortality in recipient mice with MHC (major histocompatibility complex) -mismatched HSCT. Given the importance of T cells in the development of GVHD, there is a significant gap in scientific literature regarding LRP1’s role in T cell biology. Furthermore, there is limited research interest and publications on this classical receptor molecule in other immune cell types. Herein, we endeavor to summarize existing knowledge about LRP1’s role in various immune cells to demonstrate the possibility of this receptor to serve as a novel target for anti-GVHD treatment

PR1-Specific T Cells Are Associated with Unmaintained Cytogenetic Remission of Chronic Myelogenous Leukemia After Interferon Withdrawal

Interferon-alpha (IFN) induces complete cytogenetic remission (CCR) in 20-25% CML patients and in a small minority of patients; CCR persists after IFN is stopped. IFN induces CCR in part by increasing cytotoxic T lymphocytes (CTL) specific for PR1, the HLA-A2-restricted 9-mer peptide from proteinase 3 and neutrophil elastase, but it is unknown how CCR persists after IFN is stopped.We reasoned that PR1-CTL persist and mediate CML-specific immunity in patients that maintain CCR after IFN withdrawal. We found that PR1-CTL were increased in peripheral blood of 7/7 HLA-A2+ patients during unmaintained CCR from 3 to 88 months after IFN withdrawal, as compared to no detectable PR1-CTL in 2/2 IFN-treated CML patients not in CCR. Unprimed PR1-CTL secreted IFNgamma and were predominantly CD45RA+/-CD28+CCR7+CD57-, consistent with functional naïve and central memory (CM) T cells. Similarly, following stimulation, proliferation occurred predominantly in CM PR1-CTL, consistent with long-term immunity sustained by self-renewing CM T cells. PR1-CTL were functionally anergic in one patient 6 months prior to cytogenetic relapse at 26 months after IFN withdrawal, and in three relapsed patients PR1-CTL were undetectable but re-emerged 3-6 months after starting imatinib.These data support the hypothesis that IFN elicits CML-specific CM CTL that may contribute to continuous CCR after IFN withdrawal and suggest a role for T cell immune therapy with or without tyrosine kinase inhibitors as a strategy to prolong CR in CML

Evaluation of newly generated LRP1 antibodies in different cell types: THP1 cancer cell line, human and mouse immune cells

https://openworks.mdanderson.org/sumexp22/1008/thumbnail.jp

Generation of Functional CLL-Specific Cord Blood CTL Using CD40-Ligated CLL APC

PMCID: PMC3526610This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Prognostic factors for outcomes of patients with refractory or relapsed acute myelogenous leukemia or myelodysplastic syndromes undergoing allogeneic progenitor cell transplantation

AbstractAllogeneic progenitor cell transplantation is the only curative therapy for patients with refractory acute myelogenous leukemia or myelodysplastic syndromes. To identify prognostic factors in these patients, we performed a retrospective analysis of transplantation outcomes. Patients were selected if they had undergone an allogeneic transplantation between January 1988 and January 2002 and were not in remission or first untreated relapse at the time of transplantation. A total of 135 patients were identified. The median age was 49.5 years (range, 19-75 years). At the time of transplantation, 39.3% of patients had not responded to induction therapy, 37% had not responded to first salvage therapy, and 23.7% were beyond first salvage. Forty-one patients (30%) received unrelated donor progenitor cells. Eighty patients (59%) received either a reduced-intensity or a nonmyeloablative regimen. A total of 104 (77%) of 135 patients died, with a median survival time of 4.9 months (95% confidence interval, 3.9-6.6 months). The median progression-free survival was 2.9 months (95% confidence interval, 2.5-4.2 months). A Cox regression analysis showed that Karnofsky performance status, peripheral blood blasts, and tacrolimus exposure during the first 11 days after transplantation were predictive of survival. These data support the use of allogeneic transplantation for patients with relapsed or refractory acute myelogenous leukemia/myelodysplastic syndromes and suggest that optimal immune suppression early after transplantation is essential for long-term survival even in patients with refractory myeloid leukemias