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Rheumatoid Arthritis

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Immunotoxicity, Immune Dysfunction, and Chronic Disease

Part of the book series: Molecular and Integrative Toxicology ((MOLECUL))

Abstract

Rheumatoid arthritis (RA) challenges researchers, physicians, and patients with its complexity, its impact on lives, and its refusal to respond predictably to treatment. Because we do not know what causes RA, treatment is, at this time, entirely palliative. Many environmental factors, including smoking, diet, stress, environmental chemicals, and infections, have been implicated in either the etiology or progression of RA, but none of these emerges as a distinct causative agent of RA, in general. As more data becomes available, RA appears to be a cluster of disease entities, which may have unique etiological patterns. Therefore, the best research, current and future, will subdivide RA into disease subsets based on clinical, serological, or environmental parameters. In an iterative process, once RA subsets are defined, common mechanisms may emerge that link them and help explain the complexity, thereby leading to new therapeutic or preventative approaches. This chapter attempts to set the stage for this kind of analysis, using the new paradigm of the gene/environment interaction that unites smoking and major histocompatibility complex haplotype with RA as a critical and revealing example.

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Abbreviations

ACPA:

Anticitrullinated peptide antibodies

AhR:

Aryl hydrocarbon receptor

CCP:

Cyclic citrullinated peptide

EBV:

Epstein–Barr virus

HLA:

Human leukocyte antigen

HPA:

Hypothalamic pituitary adrenal axis

HSP:

Heat shock protein

IFN:

Interferon

IL:

Interleukin

MHC:

Major histocompatibility complex

NK:

Natural killer

PAD:

Peptidylarginine deiminase

PCB:

Polychlorinated biphenyl

POP:

Persistent organic pollutants

RA:

Rheumatoid arthritis

SLE:

Systemic lupus erythematosus

TLR:

Toll-like receptor

TNF:

Tumor necrosis factor

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Authors and Affiliations

  1. Department of Biological Sciences, Idaho State University, 921 S 8th Avenue, Stop 8007, Pocatello, ID, 83209, USA

    Jean C. Pfau

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  1. Jean C. Pfau
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Correspondence to Jean C. Pfau .

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  1. College of Veterinary Medicine, Dept. Microbiology & Immunology, Cornell University, Ithaca, 14853, New York, USA

    Rodney R. Dietert

  2. National Health and Environmental Effects, Research Laboratories, US Environmental Protection Agency, Research Triangle Park, 27711, USA

    Robert W. Luebke

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Pfau, J.C. (2012). Rheumatoid Arthritis. In: Dietert, R., Luebke, R. (eds) Immunotoxicity, Immune Dysfunction, and Chronic Disease. Molecular and Integrative Toxicology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-812-2_7

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