13 Imunidade antiinfecciosa

Prévia do material em texto

*
*
Maria Imaculada Muniz-Junqueira
Imunologia Médica
*
*
Quais os mecanismos de imunidade contra o microorganismo?
Como o microorganismo escapa de nossas defesas?
Como o microorganismo agride o nosso organismo?
*
*
COMO O MICROORGANISMO AGRIDE O NOSSO ORGANISMO?
Mecanismos dependentes do microorganismo
Mecanismos dependentes da resposta do sistema imunitário
*
*
ONDE?
QUANDO? 
COMO?
POR QUE?
*
*
Vírus
Bactérias extra-celulares
Bactérias intra-celulares
Fungos
Protozoários
Helmintos
*
*
*
*
Sarampo
Mononucleose infecciosa
varicela
hepatite
*
*
 Mecanismo de indução do Interferon tipo I pelos vírus
*
*
Ação do interferon tipo I na célula vizinha
*
*
Imunidade anti-viral
*
*
Cinética da resposta antiviral
*
*
*
*
*
*
*
*
*
*
*
*
*
*
Pneumonia bacteriana
meningite
Impetigo bolhoso
Abscesso amigadaliano
*
*
*
*
*
*
*
*
*
*
*
*
hanseníase
leishmaniose
tuberculose
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
 miracídio
cercária
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
Goodridge HS, Underhill DM. Host recognition of fungal pathogens. Drug Discovery Today: Disease Mechanisms, 2008 in press
*
*
Victor Nizet. Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets. 
J Allergy Clin Immunol 2007;120:13-22.
*
*
Victor Nizet. Understanding how leading bacterial pathogens subvert innate immunity to reveal novel therapeutic targets. 
J Allergy Clin Immunol 2007;120:13-22.
*
*
COMO É O MECANISMO DE IMUNIDADE CONTRA O MICROORGANISMO?
COMO O MICROORGANISMO ESCAPA DE NOSSAS DEFESAS?
COMO O MICROORGANISMO AGRIDE O NOSSO ORGANISMO?
COMO? QUANDO? ONDE? POR QUE?
*
Mecanismo de indução do Interferon tipo I pelos vírus
*
Ação do interferon tipo I
*
Innate and adaptive immune responses against viruses. Immunity against viruses functions to prevent infection and to eradicate established infection. Innate immunity is mediated by type I IFNs, which prevent infection, and NK cells, which eliminate infected cells. Adaptive immunity is mediated by antibodies and CTLs, which also block infection and kill infected cells, respectively.
*
Cinética da resposta antiviral
*
*
*
Adaptive immune responses to extracellular microbes. Adaptive immune responses to extracellular microbes, such as bacteria, and their toxins consist of antibody production and the activation of CD4+ helper T cells. Antibodies neutralize and eliminate microbes and toxins by several mechanisms. Helper T cells produce cytokines that stimulate B cell responses, macrophage activation, and inflammation. APC, antigen-presenting cell.
*
Innate and adaptive immunity to intracellular bacteria. The innate immune response to intracellular bacteria consists of phagocytes and NK cells, interactions among which are mediated by cytokines (IL-12 and IFN-γ). The typical adaptive immune response to these microbes is cell-mediated immunity, in which T cells activate phagocytes to eliminate the microbes. Innate immunity may control bacterial growth, but elimination of the bacteria requires adaptive immunity. These principles are based largely on analysis of Listeria monocytogenes infection in mice; the numbers of viable bacteria shown on the y-axis are relative values of bacterial colonies that can be grown from the tissues of infected mice. (From Unanue ER. Studies in listeriosis show the strong symbiosis between the innate cellular system and the T-cell response. Immunological Reviews 158: 11-25, 1997.) 
*
Role of IL-12 and IFN-γ in defense against an intracellular bacterial infection. In this experiment, wild-type (normal control) mice and knockout mice lacking the p40 subunit of IL-12 or IFN-γ were infected with the intracellular bacterium M. tuberculosis by aerosol. Lungs were examined at different times after infection for the number of bacteria capable of forming colonies in culture. Normal mice control bacterial growth, mice lacking IL-12 have a reduced ability to control the infection (and die by day 60), and IFN-γ knockout mice are incapable of limiting bacterial growth (and die by day 30 to 35). Asterisks indicate the time of death. (Data courtesy of Dr. Andrea Cooper, Department of Microbiology, Colorado State University, Fort Collins.)
*
Cooperation of CD4+ and CD8+ T cells in defense against intracellular microbes. Intracellular bacteria such as L. monocytogenes are phagocytosed by macrophages and may survive in phagosomes and escape into the cytoplasm. CD4+ T cells respond to class II MHC-associated peptide antigens derived from the intravesicular bacteria. These T cells produce IFN-γ, which activates macrophages to destroy the microbes in phagosomes. CD8+ T cells respond to class I-associated peptides derived from cytosolic antigens and kill the infected cells. 
*
Role of T cells and cytokines in determining outcome of infections. Naive CD4+ T lymphocytes may differentiate into TH1 cells, which activate phagocytes to kill ingested microbes, and TH2 cells, which inhibit macrophage activation. The balance between these two subsets may influence the outcome of infections, as illustrated by Leishmania infection in mice and leprosy in humans.
*
Antigenic variation in trypanosomes. In a mouse infected experimentally with a single clone of T. rhodesiense, the blood parasite counts show cyclic waves. Each wave is due to a new antigenic variant of the parasite (labeled variants A, B, and C) that expresses a new variable surface glycoprotein (VSG, the immunodominant antigen of the parasite), and each decline is a result of a specific antibody response to that variant. (Courtesy of Dr. John Mansfield, University of Wisconsin, Madison.)
*
cercária
*
*
*