Marcus Ramsay Clark, MD

  • Professor of Medicine
    Committee on Cancer Biology
    Committee on Immunology
    Director of Medical Scientist Training Program
  • Clinical Interests: Lupus, Psoriatic Arthritis, Rheumatoid Arthritis
  • Research and Scholarly Interests: Adaptive Immunity, Autoimmunity, B Cells, chromatin organization, Developmental Biology, gene regulation, Lupus Nephritis, Molecular Biology
  • Websites: Clark Laboratory, Research Network Profile
  • Contact: mclark@uchicago.edu
  • Graduate Programs: Cancer Biology, Immunology, UChicago Biosciences

Dr. Clark’s laboratory has a long-standing interest in B cell antigen receptor (BCR) signaling and the ways in which BCR-dependent processes regulate specific cell fate decisions. In the bone marrow, Dr. Clark's research has focused on understanding how signals initiated through the pre-BCR, in conjunction with those delivered via the IL-7 receptor, coordinate cell cycle progression with immunoglobulin light chain gene recombination. This work led to the discovery of the epigenetic reader BRWD1 as a critical regulator of both Ig-kappa accessibility and the coordination of broad transcriptional programs during early and late B lymphopoiesis.



More recently, Dr. Clark’s team demonstrated that the pre-BCR initiates an IRF4-CXCR4 feedforward loop, and that CXCR4 directly signals Ig-kappa recombination. These findings fundamentally revise the canonical model of B lymphopoiesis and represent the first demonstration of a direct and independent role for CXCR4 in driving a key biological process.



In peripheral tissues, Dr. Clark has concentrated on the molecular regulation of germinal centers (GCs). His group recently identified two novel B cell populations within the dark zone that enable compartmentalization of core GC functions and uncover the molecular programs driving the GC cycle. This three-population model significantly reshapes the prevailing paradigm of GC biology. Across all areas of investigation, Dr. Clark’s laboratory has developed novel in vivo models and conducted targeted in vitro studies to achieve definitive insights into these complex processes.



On the translational front, Dr. Clark has explored how in situ adaptive immune responses contribute to tubulointerstitial inflammation in human lupus nephritis. For these studies, his group has employed deep machine learning to create innovative image analysis tools capable of quantifying and elucidating functional relationships between different T cell and antigen-presenting cell populations in situ. Notably, this bioinformatics platform achieves sensitivity and specificity approaching that of two-photon excitation microscopy (TPEM), while being applicable to the study of human disease. Additionally, Dr. Clark’s team has utilized single-cell technologies to investigate B cell selection at sites of inflammation and to examine the interplay between transcriptional state and antigenic specificity.

Pseudo-spectral angle mapping for pixel and cell classification in highly multiplexed immunofluorescence images.
Pseudo-spectral angle mapping for pixel and cell classification in highly multiplexed immunofluorescence images. J Med Imaging (Bellingham). 2024 Nov; 11(6):067502.
PMID: 39664650

BRWD1 establishes epigenetic states for germinal center initiation, maintenance, and function.
BRWD1 establishes epigenetic states for germinal center initiation, maintenance, and function. bioRxiv. 2024 Apr 28.
PMID: 38712068

Pseudo-spectral angle mapping for automated pixel-level analysis of highly multiplexed tissue image data.
Pseudo-spectral angle mapping for automated pixel-level analysis of highly multiplexed tissue image data. bioRxiv. 2024 Jan 11.
PMID: 38260318

Lineage-specific 3D genome organization is assembled at multiple scales by IKAROS.
Lineage-specific 3D genome organization is assembled at multiple scales by IKAROS. Cell. 2023 11 22; 186(24):5269-5289.e22.
PMID: 37995656

BRWD1 orchestrates small pre-B?cell chromatin topology by converting static to dynamic cohesin.
BRWD1 orchestrates small pre-B?cell chromatin topology by converting static to dynamic cohesin. Nat Immunol. 2024 Jan; 25(1):129-141.
PMID: 37985858

Corrigendum to "Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu" [J. Autoimmun. 113 (2020) 102469].
Corrigendum to "Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu" [J. Autoimmun. 113 (2020) 102469]. J Autoimmun. 2023 Nov; 140:103116.
PMID: 37748978

Molecular mechanisms insulating proliferation from genotoxic stress in B lymphocytes.
Molecular mechanisms insulating proliferation from genotoxic stress in B lymphocytes. Trends Immunol. 2023 09; 44(9):668-677.
PMID: 37573227

STAT3 signaling in B cells controls germinal center zone organization and recycling.
STAT3 signaling in B cells controls germinal center zone organization and recycling. Cell Rep. 2023 05 30; 42(5):112512.
PMID: 37200190

Antigenic responses are hallmarks of fibrotic interstitial lung diseases independent of underlying etiologies.
Antigenic responses are hallmarks of fibrotic interstitial lung diseases independent of underlying etiologies. medRxiv. 2023 May 11.
PMID: 37214861

The endogenous repertoire harbors self-reactive CD4+ T cell clones that adopt a follicular helper T cell-like phenotype at steady state.
The endogenous repertoire harbors self-reactive CD4+ T cell clones that adopt a follicular helper T cell-like phenotype at steady state. Nat Immunol. 2023 03; 24(3):487-500.
PMID: 36759711

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