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B-Cell Activation

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Immunology

Summary

The process of B-cell activation occurs within secondary lymphoid organs such as the spleen and lymph nodes. This process begins when a B-cell encounters a foreign antigen for the first time. There are two modes of B-cell activation: T-cell dependent and T-cell independent. In T-cell dependent activation, the B-cell binds to the antigen with its surface receptor, which undergoes receptor-mediated endocytosis. It then presents the antigen on a MHC class II molecule to a helper T-cell. The T-cell receptor binds to the presented antigen complex. The CD40 ligand on the helper T-cell binds to the CD40 receptor on the B-cell, providing a co-stimulatory signal. Cytokines are released by the helper T-cell, stimulating B-cell proliferation and class switching before ultimately differentiating into memory B-cells and antibody-secreting plasma cells. In contrast, T-cell independent B-cell activation can be triggered by multivalent antigens like lipopolysaccharides (LPS) or flagellin which bind to the B-cell's toll-like receptors without helper T-cell assistance.

Lesson Outline

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FAQs

What is the main function of the Complement Cascade in the immune system?

The Complement Cascade, a part of the immune system, plays a crucial role in host defense against infections. It's a complex series of enzymatic reactions involving protein cleavage, during which inactived complement proteins are systematically split apart, or cleaved, effectively "activating" them. They work to enhance the ability of the immune system to clear microbes and damaged cells, promote inflammation, and attack the pathogen's plasma membrane through the formation of a Membrane Attack Complex (MAC).

What are the three different Complement Activation Pathways?

There are three Complement Activation Pathways: Classical, Alternate and Lectin pathways. Each pathway is initiated by different stimuli, but all eventually lead to the cleavage and activation of C3, a complement protein. Once C3 is activated, the pathways converge, leading to opsonization of pathogens, inflammation, and even lysis of pathogens through the formation of the Membrane Attack Complex. The classical pathway is triggered by antibody-antigen interactions, while the lectin pathway recognizes microbial polysaccharides. The alternate pathway can be initiated spontaneously or by components of microorganisms.

What role does Complement play in Opsonization of bacteria?

Opsonization is a process in which pathogens are marked for destruction by the immune system. The Complement system contributes to opsonizaton when activated Complement proteins bind to the surface of pathogens, marking them for destruction. These 'tags' signal cells of the immune system like macrophages to engulf and destroy the pathogen. This function of the Complement system aids in effectively clearing pathogens from the body.

What is the significance of C3 Cleavage in the Complement Cascade?

C3 cleavage is a pivotal step in the Complement Cascade. The cleavage of the C3 protein yields two active fragments, C3a and C3b. C3b is involved in opsonization, enhancing the ability of phagocytic cells to engulf bacteria. Additionally, C3b contributes to the formation of C5 convertase, an enzyme vital to the initiation of the terminal pathway of the complement system, culminating in the formation of the Membrane Attack Complex. Meanwhile, C3a is an anaphylatoxin that triggers inflammation.

How does the formation of Membrane Attack Complex contribute to the function of Complement?

The Membrane Attack Complex (MAC) is a key player in combating infections. It forms when complement proteins assemble on the membrane surface of pathogenic cells, creating a pore that disrupts the cell membrane integrity. This leads to the lysis and eventual death of the pathogen. The MAC is therefore considered one of the terminal effector functions of the Complement system, directly contributing to the elimination of pathogens from the body.