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Lam L, Halder RC, Montoya DJ, et al. Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways. Am J Neurodegener Dis. 2015;4(2):28-39
Lam, L., Halder, R. C., Montoya, D. J., Rubbi, L., Rinaldi, A., Sagong, B., Weitzman, S., Rubattino, R., Singh, R. R., Pellegrini, M., & Fiala, M. (2015). Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways. American journal of neurodegenerative disease, 4(2), 28-39.
Lam, Larry, et al. "Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways." American journal of neurodegenerative disease vol. 4,2 (2015): 28-39.
Lam L, Halder RC, Montoya DJ, Rubbi L, Rinaldi A, Sagong B, Weitzman S, Rubattino R, Singh RR, Pellegrini M, Fiala M. Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways. Am J Neurodegener Dis. 2015 Dec 28;4(2):28-39. eCollection 2015. PMID: 26807342; PMCID: PMC4700124.
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Am J Neurodegener Dis. 2015 Dec 28;4(2):28-39. eCollection 2015.

Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways.

American journal of neurodegenerative disease

Larry Lam, Ramesh C Halder, Dennis J Montoya, Liudmilla Rubbi, Arturo Rinaldi, Bien Sagong, Sarah Weitzman, Rachel Rubattino, Ram Raj Singh, Matteo Pellegrini, Milan Fiala

Affiliations

  1. Department of Molecular, Cell and Developmental Biology, UCLA School of Medicine Los Angeles, CA 90095-1606.
  2. Department of Surgery, UCLA School of Medicine Los Angeles, CA 90095-7022.
  3. Department of Medicine, UCLA School of MedicineLos Angeles, CA 90095-1670; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLALos Angeles, CA 90095-1670.

PMID: 26807342 PMCID: PMC4700124

Abstract

Sporadic ALS patients display heterogeneous immune pathways in peripheral blood mononuclear cells (PBMCs). We tested nine sALS patients and one unaffected identical twin of an index case by RNA-Seq of PBMCs. The inflammatory patients (n = 3) clustered into a subset with an inflammatory Th1/Th17 signature and the non-inflammatory patients (n = 7) into another subset with a B cell signature. The inflammatory subset was remarkable for granulocyte and agranulocyte diapedesis, hepatic fibrosis, roles of cytokines and metalloproteases. The non-inflammatory subset was highlighted by degradation of vitamin E, serotonin and nucleotides, altered T cell and B cell signaling, agranulocyte diapedesis, and up regulation of B cell genes. Identification of these differentially regulated pathways in sALS patients may guide the choice of anti-inflammatory therapies.

Keywords: Amyotrophic lateral sclerosis; hepatic fibrosis; immune pathways; tocilizumab; vitamin E

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