Summary

Dr. Carmelo Carmona-Rivera participated in the identification of a novel causing-gene of the rare condition named Hermansky-Pudlak syndrome under the mentorship of Dr. William Gahl. He is currently a research fellow and focuses on the cellular, biochemistry and molecular aspects of neutrophil extracellular traps (NETs) formation and its impact in autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and vasculitis. Among his honor and awards are the American Association of Immunologist, American Society for Cell Biology and the Pan-American Society of Pigment Cell Research for his outstanding research.

Research Statement

NETosis is a neutrophil-programmed cell death characterized by the release of chromatin fibers decorated with antimicrobial peptides. This mechanism may promote externalization of autoAntigens that normally are sheltered from immune recognition. Therefore, underlying possible role of neutrophil extracellular traps (NETs) in the pathogenesis of heterogeneous autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Dr. Carmona is focused on determining factors present on NETs that trigger endothelial damage in lupus and RA. Proteins within NETs are posttranslationally modified (e.g. methylation, citrullination) creating neoantigens that may trigger and autoimmune response in SLE and other conditions. Thus, the elucidation of how posttranslational modifications present in NETs contribute to break tolerance and exacerbate the autoimmune response is another his goals.

Scientific Publications

A role for muscarinic receptors in neutrophil extracellular trap formation and levamisole-induced autoimmunity.

Carmona-Rivera C, Purmalek MM, Moore E, Waldman M, Walter PJ, Garraffo HM, Phillips KA, Preston KL, Graf J, Kaplan MJ, Grayson PC
JCI insight.
2017 Feb 9;
2(3).
doi: 10.1172/jci.insight.89780
PMID: 28194438

DEK-targeting DNA aptamers as therapeutics for inflammatory arthritis.

Mor-Vaknin N, Saha A, Legendre M, Carmona-Rivera C, Amin MA, Rabquer BJ, Gonzales-Hernandez MJ, Jorns J, Mohan S, Yalavarthi S, Pai DA, Angevine K, Almburg SJ, Knight JS, Adams BS, Koch AE, Fox DA, Engelke DR, Kaplan MJ, Markovitz DM
Nature communications.
2017 Feb 6;
8().
doi: 10.1038/ncomms14252
PMID: 28165452

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
Nature medicine.
2016 Feb;
22(2).
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
Annals of the rheumatic diseases.
2015 Jul;
74(7).
doi: 10.1136/annrheumdis-2013-204837
PMID: 24570026

A divalent interaction between HPS1 and HPS4 is required for the formation of the biogenesis of lysosome-related organelle complex-3 (BLOC-3).

Carmona-Rivera C, Simeonov DR, Cardillo ND, Gahl WA, Cadilla CL
Biochimica et biophysica acta.
2013 Mar;
1833(3).
doi: 10.1016/j.bbamcr.2012.10.019
PMID: 23103514

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
Science immunology.
2017 Apr;
2(10).
pii: eaag3358. doi: 10.1126/sciimmunol.aag3358
PMID: 28649674

Education

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

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

Experience

Research Fellow
Systemic Autoimmunity Branch, NIAMS, 2014–present

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

Last Updated: July 2020