Clinical Focus


  • Fellow
  • Allergy and Immunology
  • Primary Immunodeficiency Diseases

Academic Appointments


Professional Education


  • Doctor of Medicine, Washington University (2018)
  • Bachelor of Science, Cornell University (2009)
  • Doctor of Philosophy, Washington University (2018)
  • Board Certification, American Board of Pediatrics, Pediatrics (2022)
  • Residency, Stanford University, Pediatrics (2022)
  • PhD, Washington University, Immunology (2018)
  • MD, Washington University, Medicine (2018)

Lab Affiliations


All Publications


  • Mimickers of Classical Urticaria: Cryopyrin-Associated Autoinflammatory Syndrome Presenting as Isolated Urticaria in an Infant. The journal of allergy and clinical immunology. In practice Solomon, B. D., Skaljic, M., Liu, L. Y., Yan, D., Sheahon, K. M., Broderick, L., Hoffman, H. M., Beres, S. J., Brown, R. A., Teng, J. M., Gernez, Y. 2023

    View details for DOI 10.1016/j.jaip.2022.12.037

    View details for PubMedID 36720659

  • Prediction of HLA genotypes from single-cell transcriptome data. Frontiers in immunology Solomon, B. D., Zheng, H., Dillon, L. W., Goldman, J. D., Hourigan, C. S., Heath, J. R., Khatri, P. 2023; 14: 1146826

    Abstract

    The human leukocyte antigen (HLA) locus plays a central role in adaptive immune function and has significant clinical implications for tissue transplant compatibility and allelic disease associations. Studies using bulk-cell RNA sequencing have demonstrated that HLA transcription may be regulated in an allele-specific manner and single-cell RNA sequencing (scRNA-seq) has the potential to better characterize these expression patterns. However, quantification of allele-specific expression (ASE) for HLA loci requires sample-specific reference genotyping due to extensive polymorphism. While genotype prediction from bulk RNA sequencing is well described, the feasibility of predicting HLA genotypes directly from single-cell data is unknown. Here we evaluate and expand upon several computational HLA genotyping tools by comparing predictions from human single-cell data to gold-standard, molecular genotyping. The highest 2-field accuracy averaged across all loci was 76% by arcasHLA and increased to 86% using a composite model of multiple genotyping tools. We also developed a highly accurate model (AUC 0.93) for predicting HLA-DRB345 copy number in order to improve genotyping accuracy of the HLA-DRB locus. Genotyping accuracy improved with read depth and was reproducible at repeat sampling. Using a metanalytic approach, we also show that HLA genotypes from PHLAT and OptiType can generate ASE ratios that are highly correlated (R2 = 0.8 and 0.94, respectively) with those derived from gold-standard genotyping.

    View details for DOI 10.3389/fimmu.2023.1146826

    View details for PubMedID 37180102

  • A challenging case of recurrent idiopathic hemophagocytic lymphohistiocytosis (HLH) initially presenting in an infant with Pneumocystis jirovecii pneumonia Solomon, B., Balagtas, J., Chien, M., Pooni, R., Balboni, I., Weinacht, K., Gernez, Y. SPRINGER/PLENUM PUBLISHERS. 2021: S55
  • Helicobacter species are potent drivers of colonic T cell responses in homeostasis and inflammation. Science immunology Chai, J. N., Peng, Y., Rengarajan, S., Solomon, B. D., Ai, T. L., Shen, Z., Perry, J. S., Knoop, K. A., Tanoue, T., Narushima, S., Honda, K., Elson, C. O., Newberry, R. D., Stappenbeck, T. S., Kau, A. L., Peterson, D. A., Fox, J. G., Hsieh, C. S. 2017; 2 (13)

    Abstract

    Specific gut commensal bacteria improve host health by eliciting mutualistic regulatory T (Treg) cell responses. However, the bacteria that induce effector T (Teff) cells during inflammation are unclear. We addressed this by analyzing bacterial-reactive T cell receptor (TCR) transgenic cells and TCR repertoires in a murine colitis model. Unexpectedly, we found that mucosal-associated Helicobacter species triggered both Treg cell responses during homeostasis and Teff cell responses during colitis, as suggested by an increased overlap between the Teff/Treg TCR repertoires with colitis. Four of six Treg TCRs tested recognized mucosal-associated Helicobacter species in vitro and in vivo. By contrast, the marked expansion of luminal Bacteroides species seen during colitis did not trigger a commensurate Teff cell response. Unlike other Treg cell-inducing bacteria, Helicobacter species are known pathobionts and cause disease in immunodeficient mice. Thus, our study suggests a model in which mucosal bacteria elicit context-dependent Treg or Teff cell responses to facilitate intestinal tolerance or inflammation.

    View details for DOI 10.1126/sciimmunol.aal5068

    View details for PubMedID 28733471

    View details for PubMedCentralID PMC5684094

  • Antigen-Specific Development of Mucosal Foxp3+RORγt+ T Cells from Regulatory T Cell Precursors. Journal of immunology (Baltimore, Md. : 1950) Solomon, B. D., Hsieh, C. S. 2016; 197 (9): 3512-3519

    Abstract

    Foxp3+retinoic acid-related orphan receptor (ROR)γt+ T cells have recently been characterized as an immunoregulatory population highly enriched in the colon lamina propria. However, their developmental origin and relationship to RORγt- regulatory T and Th17 cells remain unclear. In this study, we use a fixed TCRβ system to show that the TCR repertoire of the Foxp3+RORγt+ population is mostly distinct compared with other colonic T cell subsets. However, of these TCRs, a fraction is also found in the Th17 subset, suggesting that TCR repertoire overlap may contribute to the reported ability of Foxp3+RORγt+ cells to regulate Th17 immunity. Naive transgenic T cells expressing a Foxp3+RORγt+-restricted TCR first acquire a Foxp3+RORγt- phenotype before coexpressing RORγt, suggesting that Foxp3+RORγt+ cell development can occur via an RORγt- regulatory T cell intermediate.

    View details for DOI 10.4049/jimmunol.1601217

    View details for PubMedID 27671109

    View details for PubMedCentralID PMC5101183

  • The ability to rearrange dual TCRs enhances positive selection, leading to increased Allo- and Autoreactive T cell repertoires. Journal of immunology (Baltimore, Md. : 1950) Ni, P. P., Solomon, B., Hsieh, C. S., Allen, P. M., Morris, G. P. 2014; 193 (4): 1778-86

    Abstract

    Thymic selection is designed to ensure TCR reactivity to foreign Ags presented by self-MHC while minimizing reactivity to self-Ags. We hypothesized that the repertoire of T cells with unwanted specificities such as alloreactivity or autoreactivity are a consequence of simultaneous rearrangement of both TCRα loci. We hypothesized that this process helps maximize production of thymocytes capable of successfully completing thymic selection, but results in secondary TCRs that escape stringent selection. In T cells expressing two TCRs, one TCR can mediate positive selection and mask secondary TCR from negative selection. Examination of mice heterozygous for TRAC (TCRα(+/-)), capable of only one functional TCRα rearrangement, demonstrated a defect in generating mature T cells attributable to decreased positive selection. Elimination of secondary TCRs did not broadly alter the peripheral T cell compartment, though deep sequencing of TCRα repertoires of dual TCR T cells and TCRα(+/-) T cells demonstrated unique TCRs in the presence of secondary rearrangements. The functional impact of secondary TCRs on the naive peripheral repertoire was evidenced by reduced frequencies of T cells responding to autoantigen and alloantigen peptide-MHC tetramers in TCRα(+/-) mice. T cell populations with secondary TCRs had significantly increased ability to respond to altered peptide ligands related to their allogeneic ligand as compared with TCRα(+/-) cells, suggesting increased breadth in peptide recognition may be a mechanism for their reactivity. Our results imply that the role of secondary TCRs in forming the T cell repertoire is perhaps more significant than what has been assumed.

    View details for DOI 10.4049/jimmunol.1400532

    View details for PubMedID 25015825

    View details for PubMedCentralID PMC4119549

  • T-cell selection and intestinal homeostasis. Immunological reviews Ai, T. L., Solomon, B. D., Hsieh, C. S. 2014; 259 (1): 60-74

    Abstract

    Although intestinal bacteria live deep within the body, they are topographically on the exterior surface and thus outside the host. According to the classic notion that the immune system targets non-self rather than self, these intestinal bacteria should be considered foreign and therefore attacked and eliminated. While this appears to be true for some commensal bacterial species, recent data suggest that the immune system actively becomes tolerant to many bacterial organisms. The induction or activation of regulatory T (Treg) cells that inhibit, rather than promote, inflammatory responses to commensal bacteria appears to be a central component of mucosal tolerance. Loss of this mechanism can lead to inappropriate immune reactivity toward commensal organisms, perhaps contributing to mucosal inflammation characteristic of disorders such as inflammatory bowel disease.

    View details for DOI 10.1111/imr.12171

    View details for PubMedID 24712459

    View details for PubMedCentralID PMC4028094

  • T cell immunodominance is dictated by the positively selecting self-peptide. eLife Lo, W. L., Solomon, B. D., Donermeyer, D. L., Hsieh, C. S., Allen, P. M. 2014; 3: e01457

    Abstract

    Naive T cell precursor frequency determines the magnitude of immunodominance. While a broad T cell repertoire requires diverse positively selecting self-peptides, how a single positively selecting ligand influences naive T cell precursor frequency remains undefined. We generated a transgenic mouse expressing a naturally occurring self-peptide, gp250, that positively selects an MCC-specific TCR, AND, as the only MHC class II I-E(k) ligand to study the MCC highly organized immunodominance hierarchy. The single gp250/I-E(k) ligand greatly enhanced MCC-tetramer(+) CD4(+) T cells, and skewed MCC-tetramer(+) population toward V11α(+)Vβ3(+), a major TCR pair in MCC-specific immunodominance. The gp250-selected V11α(+)Vβ3(+) CD4(+) T cells had a significantly increased frequency of conserved MCC-preferred CDR3 features. Our studies establish a direct and causal relationship between a selecting self-peptide and the specificity of the selected TCRs. Thus, an immunodominant T cell response can be due to a dominant positively selecting self-peptide. DOI: http://dx.doi.org/10.7554/eLife.01457.001.

    View details for DOI 10.7554/eLife.01457

    View details for PubMedID 24424413

    View details for PubMedCentralID PMC3885792

  • Neuropilin-1 attenuates autoreactivity in experimental autoimmune encephalomyelitis. Proceedings of the National Academy of Sciences of the United States of America Solomon, B. D., Mueller, C., Chae, W. J., Alabanza, L. M., Bynoe, M. S. 2011; 108 (5): 2040-5

    Abstract

    Neuropilin-1 (Nrp1) is a cell surface molecule originally identified for its role in neuronal development. Recently, Nrp1 has been implicated in several aspects of immune function including maintenance of the immune synapse and development of regulatory T (T(reg)) cells. In this study, we provide evidence for a central role of Nrp1 in the regulation of CD4 T-cell immune responses in experimental autoimmune encephalitis (EAE). EAE serves as an animal model for the central nervous system (CNS) inflammatory disorder multiple sclerosis (MS). EAE is mediated primarily by CD4(+) T cells that migrate to the CNS and mount an inflammatory attack against myelin components, resulting in CNS pathology. Using a tissue-specific deletion system, we observed that the lack of Nrp1 on CD4(+) T cells results in increased EAE severity. These conditional knockout mice exhibit preferential T(H)-17 lineage commitment and decreased T(reg)-cell functionality. Conversely, CD4(+) T cells expressing Nrp1 suppress effector T-cell proliferation and cytokine production both in vivo and in vitro independent of T(reg) cells. Nrp1-mediated suppression can be inhibited by TGF-β blockade but not by IL-10 blockade. These results suggest that Nrp1 is essential for proper maintenance of peripheral tolerance and its absence can result in unchecked autoreactive responses, leading to diseases like EAE and potentially MS.

    View details for DOI 10.1073/pnas.1008721108

    View details for PubMedID 21245328

    View details for PubMedCentralID PMC3033275

  • The AP-1 transcription factor Batf controls T(H)17 differentiation. Nature Schraml, B. U., Hildner, K., Ise, W., Lee, W. L., Smith, W. A., Solomon, B., Sahota, G., Sim, J., Mukasa, R., Cemerski, S., Hatton, R. D., Stormo, G. D., Weaver, C. T., Russell, J. H., Murphy, T. L., Murphy, K. M. 2009; 460 (7253): 405-9

    Abstract

    Activator protein 1 (AP-1, also known as JUN) transcription factors are dimers of JUN, FOS, MAF and activating transcription factor (ATF) family proteins characterized by basic region and leucine zipper domains. Many AP-1 proteins contain defined transcriptional activation domains, but BATF and the closely related BATF3 (refs 2, 3) contain only a basic region and leucine zipper, and are considered to be inhibitors of AP-1 activity. Here we show that Batf is required for the differentiation of IL17-producing T helper (T(H)17) cells. T(H)17 cells comprise a CD4(+) T-cell subset that coordinates inflammatory responses in host defence but is pathogenic in autoimmunity. Batf(-/-) mice have normal T(H)1 and T(H)2 differentiation, but show a defect in T(H)17 differentiation, and are resistant to experimental autoimmune encephalomyelitis. Batf(-/-) T cells fail to induce known factors required for T(H)17 differentiation, such as RORgamma t (encoded by Rorc) and the cytokine IL21 (refs 14-17). Neither the addition of IL21 nor the overexpression of RORgamma t fully restores IL17 production in Batf(-/-) T cells. The Il17 promoter is BATF-responsive, and after T(H)17 differentiation, BATF binds conserved intergenic elements in the Il17a-Il17f locus and to the Il17, Il21 and Il22 (ref. 18) promoters. These results demonstrate that the AP-1 protein BATF has a critical role in T(H)17 differentiation.

    View details for DOI 10.1038/nature08114

    View details for PubMedID 19578362

    View details for PubMedCentralID PMC2716014

  • Tpl2 kinase regulates T cell interferon-gamma production and host resistance to Toxoplasma gondii JOURNAL OF EXPERIMENTAL MEDICINE Watford, W. T., Hissong, B. D., Durant, L. R., Yamane, H., Muul, L. M., Kanno, Y., Tato, C. M., Ramos, H. L., Berger, A. E., Mielke, L., Pesu, M., Solomon, B., Frucht, D. M., Paul, W. E., Sher, A., Jankovic, D., Tsichlis, P. N., O'Shea, J. J. 2008; 205 (12): 2803-2812

    Abstract

    Tpl2 (Tumor progression locus 2), also known as Cot/MAP3K8, is a hematopoietically expressed serine-threonine kinase. Tpl2 is known to have critical functions in innate immunity in regulating tumor necrosis factor-alpha, Toll-like receptor, and G protein-coupled receptor signaling; however, our understanding of its physiological role in T cells is limited. We investigated the potential roles of Tpl2 in T cells and found that it was induced by interleukin-12 in human and mouse T cells in a Stat4-dependent manner. Deficiency of Tpl2 was associated with impaired interferon (IFN)-gamma production. Accordingly, Tpl2(-/-) mice had impaired host defense against Toxoplasma gondii with reduced parasite clearance and decreased IFN-gamma production. Furthermore, reconstitution of Rag2(-/-) mice with Tpl2-deficient T cells followed by T. gondii infection recapitulated the IFN-gamma defect seen in the Tpl2-deficient mice, confirming a T cell-intrinsic defect. CD4(+) T cells isolated from Tpl2(-/-) mice showed poor induction of T-bet and failure to up-regulate Stat4 protein, which is associated with impaired TCR-dependent extracellular signal-regulated kinase activation. These data underscore the role of Tpl2 as a regulator of T helper cell lineage decisions and demonstrate that Tpl2 has an important functional role in the regulation of Th1 responses.

    View details for DOI 10.1084/jem.20081461

    View details for Web of Science ID 000261295300014

    View details for PubMedID 19001140

    View details for PubMedCentralID PMC2585846