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1

Graham, Bird Angus, and Calvert Jane E, eds. B lymphocytes in human disease. Oxford: Oxford University Press, 1988.

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2

Finney, Michael. A study in the molecular basis of human B lymphocyte activation. Birmingham: University of Birmingham, 1991.

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3

1952-, Zouali Moncef, ed. Human B-cell superantigens. Austin: Landes, 1996.

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4

Ghaderi, Abbas Ali. Functional study of the low affinity IgE receptor (Fc[epsilon]RII/CD23) on human B lymphocytes. Birmingham: University of Birmingham, 1990.

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5

Gillis, L. Jane. Expression and recombinase activity of RAG 1 and two splice variants of RAG 2 in mature human primary tonsilar B lymphocytes. Ottawa: National Library of Canada, 1999.

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6

McGinnes, Kimberley Gay *. Analysis of human B-lymphocyte development. 1991.

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7

Rie, Menno Alexander de. Studies on in-vitro activation of human B cells. 1988.

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8

Rie, Menno Alexander de. Studies on in-vitro activation of human B cells. 1988.

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9

Talbott, Mary Catherine. The effect of vitamin B-6 supplementation on lymphocyte responsiveness in independently-living elderly persons. 1986.

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10

Talbott, Mary Catherine. The effect of vitamin B-6 supplementation on lymphocyte responsiveness in independently-living elderly persons. 1986.

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11

Human B Lymphocytes. Springer Verlag, 1986.

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12

(Editor), Manlio Ferrarini, and Federico Caligaris-Cappio (Editor), eds. Human B Cell Populations (Chemical Immunology). S. Karger Publishers (USA), 1997.

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13

Reinherz, Ellis L., Barton F. Haynes, Lee M. Nadler, and Irwin D. Bernstein. Leukocyte Typing II: Volume 2 Human B Lymphocytes. Springer, 2011.

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14

Human B Lymphocytes (Leukocyte Typing II, Vol 2). Springer, 1986.

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15

Leukocyte Typing II: Volume 2 Human B Lymphocytes. Springer, 2012.

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16

Breban, Maxime, and Hill Gaston. Immune mechanisms: adaptive immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0008.

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The role of adaptive immunity (i.e. the involvement of B and T lymphocytes) in the pathogenesis of axial spondyloarthritis has been investigated in both human disease and relevant animal models. Studies of B cell responses have not generally implicated an autoantibody in the disease, but there are abnormalities of antibody responses, particularly increased titres of antibodies to various gut bacteria. T cells are critical to the disease in animal models other than those where overexpression of a cytokine is engineered, suggesting that they are the drivers of the inflammatory response. There is convergent evidence from animal models, genetics in humans, and direct observation of human peripheral blood and joints to implicate T cells producing IL-17 under the influence of IL-23. These in turn may be responding to bacteria either in the gut or on the skin.
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