Accession Number : AD1013787

Title :   The Importance of TLR2 and Macrophages in Modulating a Humoral Response after Encountering Streptococcus pneumoniae

Descriptive Note : Technical Report

Corporate Author : Uniformed Services University Of The Health Sciences Bethesda United States

Personal Author(s) : Vasilevsky,Sam

Full Text :

Report Date : 26 Mar 2008

Pagination or Media Count : 184

Abstract : Streptococcus pneumoniae (Pn) is an important pathogen in many community-acquired infections, including acute bacterial sinusitis, community-acquired pneumonia, as well as in more invasive infections, such as meningitis and bacteremia.Toll-like receptors (TLRs) are a family of 12 transmembrane proteins that recognize pathogens and are expressed on various immune cells including macrophages (M),dendritic cells (DC), T and B, cells and they play an important role in the initial recognition of pathogens by binding conserved moieties known as pathogen associated molecular patterns (PAMPs). Pn is known to contain ligands for TLR2, TLR4, TLR7/8,and TLR9 that can act collectively to initiate innate immunity. This is largely mediated through phagocytosis and intracellular killing by neutrophils and macrophages that are recruited to, and activated at, the site of infection (1). Adaptive immunity is initiated when professional antigen-presenting cells (APCs), such as macrophages (M) and dendritic cells (DC) recognize microbial surface components via cell surface receptors(i.e. TLRs and scavenger receptors) phagocytose the bacterium, produce numerous cytokines/chemokines and migrate to secondary lymphoid organs such as the spleen and lymph nodes. Once in the secondary lymphoid tissue, the APCs activate T cells leading to many immune effector mechanisms, including the production of antibodies by B cells. In the following dissertation, I have used a murine model to study the host response to Pn.

Descriptors :   Streptococcal pneumonia , Macrophages , Humoral immunity , proteins , Pathogenic materials , Ligands

Distribution Statement : APPROVED FOR PUBLIC RELEASE