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7. B Cell Signatures Distinguish Cutaneous Lupus Erythematosus Subtypes and the Presence of Systemic Disease Activity

Author

Abernathy-Close, Lisa, primary, Lazar, Stephanie, additional, Stannard, Jasmine, additional, Tsoi, Lam C., additional, Eddy, Sean, additional, Rizvi, Syed M., additional, Yee, Christine M., additional, Myers, Emily M., additional, Namas, Rajaie, additional, Lowe, Lori, additional, Reed, Tamra J., additional, Wen, Fei, additional, Gudjonsson, Johann E., additional, Kahlenberg, J. Michelle, additional, and Berthier, Celine C., additional

Published
2021
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10. IL18-containing 5-gene signature distinguishes histologically identical dermatomyositis and lupus erythematosus skin lesions

Author

Tsoi, Lam C., primary, Gharaee-Kermani, Mehrnaz, additional, Berthier, Celine C., additional, Nault, Tori, additional, Hile, Grace A., additional, Estadt, Shannon N., additional, Patrick, Matthew T., additional, Wasikowski, Rachael, additional, Billi, Allison C., additional, Lowe, Lori, additional, Reed, Tamra J., additional, Gudjonsson, Johann E., additional, and Kahlenberg, J. Michelle, additional

Published
2020
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11. Molecular Profiling of Cutaneous Lupus Lesions Identifies Subgroups Distinct from Clinical Phenotypes

Author

Berthier, Celine C., primary, Tsoi, Lam C., additional, Reed, Tamra J., additional, Stannard, Jasmine N., additional, Myers, Emily M., additional, Namas, Rajaie, additional, Xing, Xianying, additional, Lazar, Stephanie, additional, Lowe, Lori, additional, Kretzler, Matthias, additional, Gudjonsson, Johann E., additional, and Kahlenberg, J. Michelle, additional

Published
2019
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12. Hypersensitive IFN Responses in Lupus Keratinocytes Reveal Key Mechanistic Determinants in Cutaneous Lupus

Author

Tsoi, Lam C., primary, Hile, Grace A., additional, Berthier, Celine C., additional, Sarkar, Mrinal K., additional, Reed, Tamra J., additional, Liu, Jianhua, additional, Uppala, Ranjitha, additional, Patrick, Matthew, additional, Raja, Kalpana, additional, Xing, Xianying, additional, Xing, Enze, additional, He, Kevin, additional, Gudjonsson, Johann E., additional, and Kahlenberg, J. Michelle, additional

Published
2019
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18. Staphlyococcus aureusPhenol-Soluble Modulins Stimulate the Release of Proinflammatory Cytokines from Keratinocytes and Are Required for Induction of Skin Inflammation

Author

Syed, Adnan K., Reed, Tamra J., Clark, Kaitlyn L., Boles, Blaise R., and Kahlenberg, J. Michelle

Abstract

ABSTRACTStaphylococcus aureusis a human commensal that colonizes the skin. While it is normally innocuous, it has strong associations with atopic dermatitis pathogenesis and has become the leading cause of skin and soft tissue infections in the United States. The factors that dictate the role of S. aureusin disease are still being determined. In this work, we utilized primary keratinocyte culture and an epidermal murine colonization model to investigate the role of S. aureusphenol-soluble modulins (PSMs) in proinflammatory cytokine release and inflammation induction. We demonstrated that many species of Staphylococcusare capable of causing release of interleukin 18 (IL-18) from keratinocytes and that S. aureusPSMs are necessary and sufficient to stimulate IL-18 release from keratinocytes independently of caspase 1. Further, after 7 days of epicutaneous exposure to wild-type S. aureus, but not S. aureusΔpsm, we saw dramatic changes in gross pathology, as well as systemic release of proinflammatory cytokines. This work demonstrates the importance of PSM peptides in S. aureus-mediated inflammatory cytokine release from keratinocytes in vitroand in vivoand further implicates PSMs as important contributors to pathogenesis.

Published
2015
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19. Interleukin-5 Supports the Expansion of Fas Ligand-Expressing Killer B Cells that Induce Antigen-Specific Apoptosis of CD4+ T Cells and Secrete Interleukin-10.

Author

Klinker, Matthew W., Reed, Tamra J., Fox, David A., and Lundy, Steven K.

Subjects
*FAS proteins, *LIGANDS (Biochemistry), *INTERLEUKIN-5, *B cells, *APOPTOSIS, *ANTIGENS, *T cells, *INTERLEUKIN-10, *IMMUNOREGULATION
Abstract

Beyond their critical role in humoral immunity, B lymphocytes can employ a variety of immunomodulatory mechanisms including expression of the apoptosis-inducing molecule Fas ligand (FasL; CD178). Here, we extensively characterized the surface phenotype of FasL+ killer B cells, showing they are enriched in the IgMhighCD5+CD1dhigh B cell subset previously reported to contain a higher frequency of B cells producing interleukin-10 (IL-10). A rare population of B cells expressing IL-10 was present among FasL+ B cells, but most FasL+ B cells did not produce IL-10. We also identify interleukin-5 (IL-5) as a novel inducer of killer B cell function. Constitutively FasL+ B cells expressed higher levels of the IL-5 receptor, and treating B cells with IL-5 and CD40L resulted in the expansion of a B cell population enriched for FasL+ cells. B cells stimulated with IL-5 and CD40L were potent inducers of apoptosis in activated primary CD4+ T cells, and this killing function was antigen-specific and dependent upon FasL. IL-5 also enhanced IL-10 secretion in B cells stimulated with CD40L. Taken together these findings elucidate the relationship of FasL+ B cells and IL-10-producing B cells and demonstrate that IL-5 can induce or enhance both killer B cell activity and IL-10 secretion in B cells. Finally, we found that the killer B cell activity induced by IL-5 was completely blocked by IL-4, suggesting the existence of a previously unknown antagonistic relationship between these type-2 cytokines in modulating the activity of killer B cells. Targeting this IL-5/IL-4 signaling axis may therefore represent a novel area of drug discovery in inflammatory disorders. [ABSTRACT FROM AUTHOR]

Published
2013
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21. Staphylococcus aureusColonization Is Increased on Lupus Skin Lesions and Is Promoted by IFN-Mediated Barrier Disruption

Author

Sirobhushanam, Sirisha, Parsa, Navya, Reed, Tamra J., Berthier, Celine C., Sarkar, Mrinal K., Hile, Grace A., Tsoi, Lam C., Banfield, Josh, Dobry, Craig, Horswill, Alexander R., Gudjonsson, Johann E., and Kahlenberg, J. Michelle

Abstract

Cutaneous inflammation is recurrent in systemic lupus erythematosus (SLE), yet mechanisms that drive cutaneous inflammation in SLE are not well defined. Type I IFNs are elevated in nonlesional SLE skin and promote inflammatory responses. Staphylococcus aureus, known to induce IFN production, could play a role in cutaneous inflammation in SLE. We show here that active cutaneous lupus erythematosus lesions are highly colonized (∼50%) by S. aureus. To define the impact of IFNs on S. aureuscolonization, we examined the effects of type I and type II IFNs on S. aureusadherence and invasion. An increase in adherent S. aureuswas observed after exposure to both IFN-α and -γ, whereas IFN-γ appeared to inhibit invasion of S. aureus. Cutaneous lupus erythematosus lesional skin microarray data and RNA sequencing data from SLE keratinocytes identified repression of barrier gene expression, such as filaggrin and loricrin, and SLE keratinocytes exhibited increased S. aureus–binding integrins. These SLE-associated changes could be replicated by IFN treatment of keratinocytes. Further, SLE keratinocytes exhibited increased binding to S. aureus.Together, these data suggest that chronic exposure to IFNs induces barrier disruption that allows for higher S. aureuscolonization in SLE skin.

Published
2020
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