About

Ian Mullins is an Associate Professor of Sociology and a member of the General Faculty at the University of Virginia. His research interests include politics, culture, and ignorance, with a focus on conservative politics in the United States. He employs ethnographic and historical methods to investigate the cultural practices through which conservatives produce knowledge and come to see particular information as truthful or trustworthy. Mullins is working on a book-length manuscript that explores the historical linkages between the conservative movement in the twentieth century and the current crisis of public knowledge, analyzing how this history influences the ways individuals involved in contemporary conservative political organizations produce and validate truth claims. He earned his Ph.D. in Sociology from the University of California San Diego in 2018, his M.A. in Sociology from California State University at Northridge in 2007, and his B.A. in American Studies and Sociology from the University of Minnesota in 2005.

Research topics

• Immunology
• Virology
• Cancer research
• Biology
• Medicine
• Biochemistry
• Molecular biology

Selected publications

• Supplementary Figure 2 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023

  • Immunology
  • Medicine
  • Virology

  <p>PDF file - 548K, Supplemental Figure 2: Representative staining for surface and intracellular CXCR3.</p>

  PublisherDOI

• Supplementary Figure 2 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023-04-03

  preprintOpen access

  <p>PDF file - 548K, Supplemental Figure 2: Representative staining for surface and intracellular CXCR3.</p>

  PublisherOA PDFDOI

• Supplementary Legend from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  2023-03-30

  preprintOpen access1st authorCorresponding

  Supplementary Legend from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  PublisherOA PDFDOI

• Data from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023-04-03

  preprintOpen access

  <div>Abstract<p>T-cell infiltration of melanoma is associated with enhanced clinical efficacy and is a desirable endpoint of immunotherapeutic vaccination. Infiltration is regulated, in part, by chemokine receptors and selectin ligands on the surface of tumor-specific lymphocytes. Therefore, we investigated the expression of two homing molecules, CXC chemokine receptor 3 (CXCR3) and cutaneous lymphocyte antigen (CLA), on vaccine-induced CD8 T cells, in the context of a clinical trial of a melanoma-specific peptide vaccine. Both CXCR3 and CLA have been associated with T-cell infiltration of melanoma. We show that a single subcutaneous/intradermal administration of peptide vaccine in Montanide adjuvant induces tumor-specific CD8 T cells that are predominantly positive for CXCR3, with a subpopulation of CXCR3<sup>+</sup>CLA<sup>+</sup> cells. Addition of granulocyte macrophage colony—stimulating factor (GM-CSF) significantly enhances CXCR3 expression and increases the proportion of CLA-expressing cells. Concurrent with CXCR3 and CLA expression, vaccine-induced CD8 cells express high levels of T-bet, IFN-γ, and interleukin-12 receptor (IL-12Rβ1). Collectively, these studies show that peptide vaccination in adjuvant induces CD8 T cells with a phenotype that may support infiltration of melanoma. <i>Cancer Immunol Res; 1(5); 332–9. ©2013 AACR</i>.</p></div>

  PublisherDOI

• Supplementary Legend from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  2023-03-30

  preprintOpen access1st authorCorresponding

  Supplementary Legend from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  PublisherDOI

• Supplementary Figure 3 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023-04-03

  preprintOpen access

  <p>PDF file - 551K, Supplemental Figure 3: Representative CXCR3 and CLA staining in tetramer-negative cell populations.</p>

  PublisherDOI

• Supplementary Table 1 from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023-04-03

  supplementary-materialsOpen access

  <p>PDF file - 45K, Supplemental Table I: Effect of GM-CSF in vaccine on the expression of CXCR3 and CLA by tetramer-positive CD8+ T cells.</p>

  PublisherDOI

• Data from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  2023-03-30

  preprintOpen access1st authorCorresponding

  <div>Abstract<p>Despite the presence of tumor Ag-specific CD8<sup>+</sup> T cells in the peripheral blood, metastatic melanoma often evades immune-mediated destruction. Even after therapeutic efforts to expand Ag-specific T-cell populations, the correlation between magnitude of response and clinical efficacy has been weak. Because the migratory phenotype of tumor Ag-specific effector T cells may determine their ability for tumor control, we hypothesized that the expression of CC or CXC chemokine receptor (CCR) molecules on activated CD8<sup>+</sup> T cells may define phenotypes associated with more effective control of melanoma progression and prolonged survival. In a retrospective evaluation of patient isolates, CCR expression was determined for activated CD8<sup>+</sup> T cells derived from the peripheral blood or tumor-involved lymph nodes of 52 patients with stage III or IV metastatic melanoma. In patients with stage III disease, expression of CXCR3 by CD8<sup>+</sup>CD45RO<sup>+</sup> cells was significantly associated with enhanced survival. This was a stage-specific effect, because it was not observed in patients with stage IV disease. In addition, CCR4 and CXCR3 were highly coexpressed and associated with enhanced survival in stage III patients; however, CXCR3 seems to be the dominant receptor associated with clinical outcome. These findings support the hypothesis that the host immune system affects cancer progression and control, and that measures of CCR status of circulating lymphocytes may have prognostic value.</p></div>

  PublisherDOI

• Data from CXC Chemokine Receptor 3 Expression by Activated CD8<sup>+</sup> T cells Is Associated with Survival in Melanoma Patients with Stage III Disease

  2023-03-30

  preprintOpen access1st authorCorresponding

  <div>Abstract<p>Despite the presence of tumor Ag-specific CD8<sup>+</sup> T cells in the peripheral blood, metastatic melanoma often evades immune-mediated destruction. Even after therapeutic efforts to expand Ag-specific T-cell populations, the correlation between magnitude of response and clinical efficacy has been weak. Because the migratory phenotype of tumor Ag-specific effector T cells may determine their ability for tumor control, we hypothesized that the expression of CC or CXC chemokine receptor (CCR) molecules on activated CD8<sup>+</sup> T cells may define phenotypes associated with more effective control of melanoma progression and prolonged survival. In a retrospective evaluation of patient isolates, CCR expression was determined for activated CD8<sup>+</sup> T cells derived from the peripheral blood or tumor-involved lymph nodes of 52 patients with stage III or IV metastatic melanoma. In patients with stage III disease, expression of CXCR3 by CD8<sup>+</sup>CD45RO<sup>+</sup> cells was significantly associated with enhanced survival. This was a stage-specific effect, because it was not observed in patients with stage IV disease. In addition, CCR4 and CXCR3 were highly coexpressed and associated with enhanced survival in stage III patients; however, CXCR3 seems to be the dominant receptor associated with clinical outcome. These findings support the hypothesis that the host immune system affects cancer progression and control, and that measures of CCR status of circulating lymphocytes may have prognostic value.</p></div>

  PublisherDOI

• Data from Peptide Vaccination in Montanide Adjuvant Induces and GM-CSF Increases CXCR3 and Cutaneous Lymphocyte Antigen Expression by Tumor Antigen–Specific CD8 T Cells

  2023-04-03

  preprintOpen access

  <div>Abstract<p>T-cell infiltration of melanoma is associated with enhanced clinical efficacy and is a desirable endpoint of immunotherapeutic vaccination. Infiltration is regulated, in part, by chemokine receptors and selectin ligands on the surface of tumor-specific lymphocytes. Therefore, we investigated the expression of two homing molecules, CXC chemokine receptor 3 (CXCR3) and cutaneous lymphocyte antigen (CLA), on vaccine-induced CD8 T cells, in the context of a clinical trial of a melanoma-specific peptide vaccine. Both CXCR3 and CLA have been associated with T-cell infiltration of melanoma. We show that a single subcutaneous/intradermal administration of peptide vaccine in Montanide adjuvant induces tumor-specific CD8 T cells that are predominantly positive for CXCR3, with a subpopulation of CXCR3<sup>+</sup>CLA<sup>+</sup> cells. Addition of granulocyte macrophage colony—stimulating factor (GM-CSF) significantly enhances CXCR3 expression and increases the proportion of CLA-expressing cells. Concurrent with CXCR3 and CLA expression, vaccine-induced CD8 cells express high levels of T-bet, IFN-γ, and interleukin-12 receptor (IL-12Rβ1). Collectively, these studies show that peptide vaccination in adjuvant induces CD8 T cells with a phenotype that may support infiltration of melanoma. <i>Cancer Immunol Res; 1(5); 332–9. ©2013 AACR</i>.</p></div>

  PublisherDOI

Frequent coauthors

• Craig L. Slingluff

  University of Virginia

  17 shared

• David W. Mullins

  Dartmouth College

  17 shared

• Laura K. King

  9 shared

• Eleanor Clancy‐Thompson

  AstraZeneca (United States)

  9 shared

• William A. Knaus

  9 shared

• Melanie E. Mayer

  8 shared

• Lenora D. Nunnley

  8 shared

• Sara G. Anderson

  8 shared