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Molecular Biology of the Cell by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter by by Bruce Alberts, Alexander Johnson, Julian Lewis, David Morg

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B CELLS AND IMMUNOGLOBULINS

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Myasthenia gravis is an example of such an autoimmune disease. Most of the

affected individuals make antibodies against the acetylcholine receptors on their

own skeletal muscle cells; these receptors are required for the muscle to contract

normally in response to nerve stimulation, which releases acetylcholine (see Figure

11–39). The antibodies interfere with the normal functioning of the receptors

so that the patients become weak and may die because they cannot breathe. Similarly,

in juvenile (type 1) diabetes, adaptive immune reactions against insulin-secreting

β cells in the pancreas kill these cells, leading to severe insulin deficiency.

Summary

Innate immune responses triggered by pathogens at sites of infection help activate

adaptive immune responses in peripheral lymphoid organs. The adaptive immune

system is composed of many millions of B and T cell clones, with the cells in each

clone sharing a unique cell-surface receptor that enables them to bind a particular

pathogen antigen. The binding of antigen to these receptors, with the help of

co-stimulatory signals, stimulates the lymphocyte to proliferate and differentiate

into an effector cell that can help eliminate the pathogen. Effector B cells secrete

antibodies, which can act over long distances to help eliminate extracellular

pathogens and their toxins. Effector T cells, by contrast, produce cell-surface and

secreted co-stimulatory molecules, which mainly act locally to help other immune

cells eliminate the pathogen; in addition, some T cells can induce infected host cells

to kill themselves.

During a primary adaptive immune response to an antigen, lymphocytes that

recognize the antigen proliferate so that there are more of them to respond the next

time, during a secondary response to the same antigen; moreover, during a primary

response, some lymphocytes differentiate into memory cells, which can respond

faster and more efficiently the next time the same pathogen invades. These two

mechanisms are largely responsible for immunological memory. Both B and T cells

circulate continuously between one peripheral lymphoid organ and another via the

blood and lymph; only if they encounter their specific foreign antigen in a peripheral

lymphoid organ do they stop migrating, proliferate, and differentiate into effector

cells or memory cells. Lymphocytes that would react against self molecules either

alter their receptors (in the case of B cells) or are eliminated or inactivated; they can

also be suppressed by regulatory T cells. These mechanisms collectively are responsible

for immunological self-tolerance, which ensures that the adaptive immune

system normally avoids attacking the molecules and cells of the host.

B CELLS AND IMMUNOGLOBULINS

Vertebrates inevitably die of infection if they are unable to make antibodies.

Antibodies are secreted proteins that defend us against extracellular pathogens

in several ways. They bind to viruses and microbial toxins, thereby preventing

them from binding to and damaging host cells (see Figure 24–2). When bound

to an extracellular pathogen or its products, antibodies also recruit some of the

components of the innate immune system, including various types of leukocytes

and components of the complement system, which work together to inactivate or

eliminate the invaders.

Synthesized exclusively by B cells, antibodies are produced in billions of forms,

each with a different amino acid sequence. They belong to the class of proteins

called immunoglobulins (abbreviated as Igs) and are among the most abundant

protein components in the blood. In this section, we discuss the structure and

function of immunoglobulins and how they are made in so many different forms.

B Cells Make Immunoglobulins (Igs) as Both Cell-Surface Antigen

Receptors and Secreted Antibodies

The first Igs made by a newly formed B cell are not secreted but are instead

inserted into the plasma membrane, where they serve as receptors for antigen.

They are called B cell receptors (BCRs), and each B cell has approximately 10 5 of

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