Carmelo Carmona-Rivera, Ph.D., received his doctoral degree from the University of Puerto Rico, School of Medicine, where he worked on the biochemistry aspects of a genetic condition called Hermansky-Pudlak syndrome (HPS). Subsequently, Dr. Carmona-Rivera participated in research under the mentorship of Dr. William Gahl at NHGRI that identified a novel causing-gene of HPS. He joined the Systemic Autoimmunity Branch at the NIAMS in 2013, where he is now a Staff Scientist.

Dr. Carmona-Rivera focuses on the cellular, biochemical, and molecular aspects of neutrophil extracellular trap (NET) formation and its impact on autoinflammatory/autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), vasculitis, and hidradenitis suppurativa (HS). He has led research involving identifying important players in joint degradation in RA, signatures/pathways involved in HS skin manifestation, and NET-related proteins implicated in organ damage in SLE.

Among his honors and awards are the NIH Merit Award in 2019 for his contribution to the understanding of autoimmune diseases, the Young Investigator Award from the Neutrophil Conference in 2018, and multiple awards from the NIAMS for his outstanding research.

Research Statement

Neutrophil extracellular trap (NET) formation is a neutrophil-programmed cell death characterized by the release of chromatin fibers decorated with granule, cytoplasmic, and enzymatic proteins. This mechanism may promote the exposure of autoantigens normally sheltered from immune recognition. The possible underlying role of NETs in the pathogenesis of autoinflammatory or autoimmune conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and hidradenitis suppurativa (HS) is a major research focus.

Specifically, Dr. Carmona-Rivera studies how NETs promote adaptive immune dysregulation and organ damage. Proteins within NETs are post-translationally modified ( for example, via citrullination, carbamylation, ubiquitination, etc.), creating neoantigens that may trigger an autoimmune response leading to autoantibody formation. Dr. Carmona-Rivera also has an interest in exploring how post-translational modifications present in NETs contribute to the development of autoimmune responses and end-organ damage.

Scientific Publications

Somatic Mutations in UBA1 and Severe Adult-Onset Autoinflammatory Disease.

Beck DB, Ferrada MA, Sikora KA, Ombrello AK, Collins JC, Pei W, Balanda N, Ross DL, Ospina Cardona D, Wu Z, Patel B, Manthiram K, Groarke EM, Gutierrez-Rodrigues F, Hoffmann P, Rosenzweig S, Nakabo S, Dillon LW, Hourigan CS, Tsai WL, Gupta S, Carmona-Rivera C, Asmar AJ, Xu L, Oda H, Goodspeed W, Barron KS, Nehrebecky M, Jones A, Laird RS, Deuitch N, Rowczenio D, Rominger E, Wells KV, Lee CR, Wang W, Trick M, Mullikin J, Wigerblad G, Brooks S, Dell'Orso S, Deng Z, Chae JJ, Dulau-Florea A, Malicdan MCV, Novacic D, Colbert RA, Kaplan MJ, Gadina M, Savic S, Lachmann HJ, Abu-Asab M, Solomon BD, Retterer K, Gahl WA, Burgess SM, Aksentijevich I, Young NS, Calvo KR, Werner A, Kastner DL, Grayson PC
N Engl J Med.
2020 Dec 31;
doi: 10.1056/NEJMoa2026834
PMID: 33108101

Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis.

O'Neil LJ, Barrera-Vargas A, Sandoval-Heglund D, Merayo-Chalico J, Aguirre-Aguilar E, Aponte AM, Ruiz-Perdomo Y, Gucek M, El-Gabalawy H, Fox DA, Katz JD, Kaplan MJ, Carmona-Rivera C
Sci Adv.
2020 Oct;
doi: 10.1126/sciadv.abd2688
PMID: 33115748

Neutrophil extracellular traps, B cells, and type I interferons contribute to immune dysregulation in hidradenitis suppurativa.

Byrd AS, Carmona-Rivera C, O'Neil LJ, Carlucci PM, Cisar C, Rosenberg AZ, Kerns ML, Caffrey JA, Milner SM, Sacks JM, Aliu O, Broderick KP, Reichner JS, Miller LS, Kang S, Robinson WH, Okoye GA, Kaplan MJ
Sci Transl Med.
2019 Sep 4;
pii: eaav5908. doi: 10.1126/scitranslmed.aav5908
PMID: 31484788

Deficiency of adenosine deaminase 2 triggers adenosine-mediated NETosis and TNF production in patients with DADA2.

Carmona-Rivera C, Khaznadar SS, Shwin KW, Irizarry-Caro JA, O'Neil LJ, Liu Y, Jacobson KA, Ombrello AK, Stone DL, Tsai WL, Kastner DL, Aksentijevich I, Kaplan MJ, Grayson PC
2019 Jul 25;
doi: 10.1182/blood.2018892752
PMID: 31015188

Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis.

Carmona-Rivera C, Carlucci PM, Moore E, Lingampalli N, Uchtenhagen H, James E, Liu Y, Bicker KL, Wahamaa H, Hoffmann V, Catrina AI, Thompson P, Buckner JH, Robinson WH, Fox DA, Kaplan MJ
Sci Immunol.
2017 Apr;
pii: eaag3358. doi: 10.1126/sciimmunol.aag3358
PMID: 28649674

NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.

Khandpur R, Carmona-Rivera C, Vivekanandan-Giri A, Gizinski A, Yalavarthi S, Knight JS, Friday S, Li S, Patel RM, Subramanian V, Thompson P, Chen P, Fox DA, Pennathur S, Kaplan MJ
Sci Transl Med.
2013 Mar 27;
doi: 10.1126/scitranslmed.3005580
PMID: 23536012

Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease.

Lood C, Blanco LP, Purmalek MM, Carmona-Rivera C, De Ravin SS, Smith CK, Malech HL, Ledbetter JA, Elkon KB, Kaplan MJ
Nat Med.
2016 Feb;
doi: 10.1038/nm.4027
PMID: 26779811

Neutrophil extracellular traps induce endothelial dysfunction in systemic lupus erythematosus through the activation of matrix metalloproteinase-2.

Carmona-Rivera C, Zhao W, Yalavarthi S, Kaplan MJ
Ann Rheum Dis.
2015 Jul;
doi: 10.1136/annrheumdis-2013-204837
PMID: 24570026


University of Puerto Rico, School of Medicine
Ph.D., Biochemistry

University of Puerto Rico, Mayagüez Campus
B.S., Industrial Microbiology


Staff Scientist
Systemic Autoimmunity Branch, NIAMS, 2018-Present

Research Fellow
Systemic Autoimmunity Branch, NIAMS, 2014–2018

Postdoctoral Fellow
Systemic Autoimmunity Branch, NIAMS, 2013–2014

Postdoctoral Fellow
University of Michigan, 2011–2013

Postdoctoral Fellow 
National Human Genome Research Institute (NHGRI), NIH, 2008–2011

Visiting Fellow
Institut Curie, France, 2006

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