Chiorazzi Figure 2.
Chiorazzi Figure 2. Hypothetical model for the promoting roles of antigen stimulation and accessory signals in B-cell chronic lymphocytic leukemia (B-CLL). / [Left] B cells from U-CLL may be stimulated by binding (auto)antigen to the BCR. The balance of negative and positive signals delivered via the BCR and survival signals transduced by IgD and delivered by other cells, cytokines, and chemokines determine whether the leukemic cell proliferates or dies by apoptosis. / [Right] B cells from M-CLL are less capable of triggering apoptosis, survival, or proliferation either due to significantly diminished ability to bind antigen because of changes in the structure of the BCR (clonal ignorance), unavailability of antigen, or defective BCR signaling, despite adequate binding of antigen (anergy; green diamond-shaped antigen). / Republished, with permission, from Chiorazzi N, et al. N Engl J Med 2005: 352: 804–815. Copyright © 2005 Massachusetts Medical Society. All rights reserved.

Hypothetical model for the promoting roles of antigen stimulation and accessory signals in B-cell chronic lymphocytic leukemia (B-CLL).

[Left] B cells from U-CLL may be stimulated by binding (auto)antigen to the BCR. The balance of negative and positive signals delivered via the BCR and survival signals transduced by IgD and delivered by other cells, cytokines, and chemokines determine whether the leukemic cell proliferates or dies by apoptosis.

[Right] B cells from M-CLL are less capable of triggering apoptosis, survival, or proliferation either due to significantly diminished ability to bind antigen because of changes in the structure of the BCR (clonal ignorance), unavailability of antigen, or defective BCR signaling, despite adequate binding of antigen (anergy; green diamond-shaped antigen).

Republished, with permission, from Chiorazzi N, et al. N Engl J Med 2005: 352: 804–815. Copyright © 2005 Massachusetts Medical Society. All rights reserved.

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