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Galerie de cartes mentales Immune response

Immune response

The immune response is the body's defense mechanism against foreign substances, such as pathogens, toxins, or damaged cells. It is a complex and coordinated process involving various cells, tissues, and organs. This mind map aims to explore the various components and processes involved in the immune response. By visualizing these interconnected elements, we can gain a deeper understanding of how the immune system functions to maintain our health and well-being.

Modifié à 2022-05-30 02:44:02

Becky D

Immune response

Becky D

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Immune Response

This is protection from infectious pathogens

Two Mechanisms

a. Innate Immunity (natural)

present BEFORE infection, evolve to recognize microbes

b. Adaptive Immunity (acquired, specific)

Stimulated by microbes

Recognizes antigens

1. Innate Immunity Components

1. Epithelial barriers

2. Phagocytes (Macrophages, Neutrophils)

3. Natural Killer cells (NK cells)

4. Plasma proteins & Complement

2. Adaptive Immunity (Making antigen receptors on T & B lymphocytes by gene rearrangements)

2 Types

Humoral Immunity (B-lymphocytes)

Cell mediated Immunity (T-lymphocytes)

T Lymphocytes

in blood (60-70% lymph), lymph nodes, spleen

act on INTRAcellular antigens

Each T cells have specific Ag receptors "TCR"

Ag presented to them, bound to MHC molecules on "Ag presenting cell" APC

(2 types)

1. T-helper cells (CD4) (Master Regulators, release Cytokines)

Cytokines influence other immune cells

2. Cytotoxic T cells (CD8) (Killers, effector cells)

B Lymphocytes

Mature B cells in blood (10-20% lymphocytes), lymph nodes, spleen, tonsils, GI

After stimulated by Ag, B cells develop plasma cells, secrete immunoglobulin

For EXTRcellular pathogens & toxins

Immunoglobulins

Made by B-cells, bind to & inactivate Ag

I(GAMED)

Macrophages

part of Mononuclear Phagocyte System

Jobs

1. Process microbes & present to T-cells (APC)

2. important Effector cells in CMI & HI response

Opsoninization, DTH

Natural Killer Cells (Part of innate)

(10-15% of peripheral Lymphocytes)

Larger than Mature Lymphocytes, have cytoplasmic granules

Granulocytes (in all types of inflammation)

Effectors in innate immune response

Neutrophils, Eosinophils, Basophils

Major Histocompatibility Molecules

Major action: bind peptide fragments (of foreign proteins), present to Ag-specific T cells

2 CLASSES

MHC I

on ALL nucleated cells & platelets

Bind + display proteins made in cell (Viral Ag)

CD8+ T-cells recognize peptides presented as MHC I molecules

MHC II

on Ag presenting cells (Macrophages, Dendritic cells & B-cells)

CD4+ helper cells only recognize these molecules if bound to MHC-II molecules

Acquired Immunodeficiency Syndrome (AIDS)

Caused by retrovirus (HIV)

Profound Immunosuppression

Opportunistic infections

Secondary Neoplasms

Neurologic Manifestation

First recognized in USA (1981), homosexuals

- 1983, HIV isolated - 1985, ELISA test

Etiology

HIV - Lentivirus Family

Two forms - HIV 1 (US, Europe, Central Africa) - HIV 2 (West Africa, India)

HIV 1

M (Major) - several subtypes A to K (no I)

O (Outlier)

N (not M or O)

Ethiopia HIV-1 M clade C

Transmission

Sexual Contact (hetero & homo)

Blood/ products

Mother to Child - intrapartum (delivery, most common) - perinatally - breast milk

Pathogenesis (Major targets > Immune System, CNS)

HIV enters thru mucosal surfaces / blood

Affects - T cells - Dendritic cells & Macrophages

Immunosuppression affects CMI

From - CD4 (Loss & infection) - Impairment of surviving T helper cells

Also affects Macrophages & Dendritic cells

Infection in lymphoid tissues, where virus is latent

Mechanisms of T-Cell immunodeficiency

Viral replication brings lysis of CD4 cells - 100 billion new viral particles - 1-2 billion CD4 T-cells die/day

- Early, Immune system replaces dying cells - Late, can't keep up with loss

Also defect in QUALITY of T cells

in lymphoid tissue, CD4 T cells, Macrophages, Follicular dendritic cells

MAJOR sites of HIV infection & persistence

CNS, Macrophages & Microglia cells infected

Neuropathogenesis

Major target for HIV infection, NS

Monocytes bring infection to CNS >> infect Macrophages & Microglial cells

Neuron are spared (thank goodness lol)

Mechanisms

1. Indirectly, by viral products

2. Soluble HIV gp120

3. Soluble factors by infected microglia - IL-1, TNF, IL-6

Natural History of HIV infection

1. Acute retroviral Syndrome

High Viremia, widespread seeding of Lymphoid tissues

40-90% individuals develop this in 3-6 weeks after infection

Non-specific Symptoms (flue like symptoms) - Fever, Weight loss, Fatigue, Sore throat, rash

Diarrhea & Vomiting sometimes

2. Middle (Chronic) Syndrome (Clinical Latency)

Immunity intact, BUT HIV replicates in Lymphoid tissues (maybe several years)

Usually ASYMPTOMATIC, sometimes PDL (Persistent Generalized Lymphadenopathy)

3. Full blown AIDS (breakdown of host defense)

Clinical Disease

Fatigue, Weight Loss, Diarrhea

- Serious opportunistic Infections - Secondary Neoplasms

w/o treatment, AIDS in 7-10 years