Immune System Overview

The presence of Memory B-Cells from the first immune response.

Humoral and Cellular Immunity.

They destroy intracellular pathogens.

Proteins made by cells that affect the behavior of other cells.

Antibodies against soluble antigens.

They protect uninfected cells by stimulating them to synthesize proteins that interfere with viral replication.

They induce apoptosis of body cells with viruses, intracellular bacteria, or cancerous traits.

They increase the body's thermostat.

Proteins that either attack microbes directly or reduce their reproductive ability.

A group of over 35 cytokines that act on leukocytes and are primarily produced by Helper T-Lymphocytes.

To induce chemotaxis (migration) in nearby cells.

A group of over 30 small pro-enzymes produced by the liver, distributed through blood and tissues.

C1 reacts with antibodies that have bound an antigen.

The inflammatory response and activation of other lymphocytes/macrophages.

Via serum.

Activation of Toll-Like Receptors (TLRs).

Malignant cells and cells infected by intracellular pathogens (viruses/bacteria).

They attract macrophages and natural killer (NK) cells to destroy infected cells.

Cytokines.

A diverse array of molecules and trillions of immune cells, especially lymphocytes.

Lymphoid tissues and circulate in body fluids.

It attracts phagocytic cells to the area, facilitating chemotaxis.

By enhancing the uptake of complement-coated antigens by antigen-presenting cells and the response of B-cells to these antigens.

It is much quicker and has a higher antibody yield.

Antigens.

Pyrogens.

By binding with specific cytokine receptors.

Large, granular, lymphoid-derived cells.

Physical trauma, intense heat, bad chemicals, or infection.

A functional system rather than an anatomical or organ-based system.

Macrophages, Neutrophils, and Lymphocytes.

Heat, redness, pain, and swelling.

They trap bacteria and prevent their entry into the body.

It is systemic; immunity isn't restricted to the initial infection site.

The ability of a microorganism to cause disease.

Large phagocytic cells derived from bone marrow that engulf and kill microorganisms.

Bacteria that cause disease in a compromised host.

They release toxic chemicals into the extracellular fluid, killing both the target and themselves.

To neutralize toxins and infectious organisms, can be transferred from one individual to another via serum

12 days in tissues or 30 minutes in blood.

Histamine, serotonin, and prostaglandins, which increase inflammation and capillary permeability.

They are critical for the synthesis of Acute Phase Proteins and mobilizing neutrophils from bone marrow.

It is a chemokine that attracts granulocytes, monocytes, and CD8+ T-cells.

IFN-gamma (Interferon-gamma).

To provide specific responses to pathogens and develop memory.

Antibody-mediated immunity.

Increases metabolic rate, kills microbes, and speeds up repair.

They neutralize bacteria, toxins, and viruses, marking them for destruction by phagocytes or complement.

Cytokines produced by lymphocytes, typically T-cells, that attract other immune cells to an infected site.

Autocrine, paracrine, and endocrine manners.

Their ability to enter circulation and their half-life in blood.

It creates a pore in the plasma membrane of bacteria, leading to lysis of antibody-coated cells.

It induces local inflammatory response, has pyrogenic action on the hypothalamus, and helps contain infection.

A microorganism that is able to cause disease.

It kills microbes on the skin, vagina, and stomach.

They are the most numerous granulocyte, making up 40-75% of blood samples, and are the most important granulocyte.

Humoral immunity and cell-mediated immunity.

Pro-inflammatory cytokines and chemokines.

TLRs and PRRs on macrophages and dendritic cells recognize PAMPs on antigens and engulf them via phagocytosis. The antigen is processed and parts are displayed on cell surfaces. Macrophages and damaged epithelia secrete pro-inflammatory cytokines to attract more immune cells

Active T-cells and secreted antibodies leave the lymph node to fight the infection via the lymph and blood.

T-Cells are unable to independently recognize antigens.

It is non-specific and responds rapidly.

Phagocytes and Natural Killer (NK) cells.

Adaptive immunity.

Patterns (PAMPs) on foreign organisms.

It prevents the entry of pathogens.

By latching onto invaders and inducing apoptosis.

Potent chemicals.

They target all cells that lack 'self' surface receptors (non-specific).

In blood and lymph.

It has pyrogenic action on the hypothalamus, stimulates the acute phase response in the liver, and activates lymphocytes during antigen presentation.

Directly by cell attack or indirectly by releasing mobilizing chemicals and antibody molecules.

They sweep bacteria into the mouth to be swallowed.

It acts as an opsonizing agent for microbes and activates the lectin pathway in the complement cascade.

It serves as a useful marker of inflammation.

They engulf and kill them.

When an organism breaches a body surface.

They are involved in anti-parasite and anti-fungal roles, weakly phagocytic, and can kill extracellular organisms by excreting toxic chemicals.

Activated dendritic cells migrate to lymph nodes, activating naive T-cells, which then activate naive B-cells to secrete antibodies.

They increase phagocyte migration to the site of infection.

Dendritic Cell.

Surface barriers like skin and epithelia.

T-helper cells, T-cytotoxic cells, and NK cells.

Through their immunoglobulin-based surface receptors.

It is stimulated via one of three pathways: Classical, Alternative, and MB-Lectin.

The process where C3b targets foreign particles for phagocytosis.

Infectious microorganisms, cancer cells, transplanted organs, grafts, and other foreign material.

Lysozyme.

It traps bacteria in the digestive and respiratory tracts.

It has memory.

The immune response wanes off following the elimination of antigens.

The immune system is non-reactive to self-antigens.

It tremendously amplifies the inflammatory response.

They scavenge dead cells, induce inflammation, and present antigens to T-helper cells.

Route of entry, number of pathogens, and immune status of the host.

Hypersensitivity and allergic reactions.

They engulf and process antigens, then present fragments on their surfaces for recognition by T-Cells.

They have pyrogenic effects.

Monocytes, macrophages, and injured epithelium.

The T-Cells leave the lymph nodes and travel to the site of infection.

No.

Proteins produced by the liver in response to inflammatory cytokines.

It acts as an opsonizing agent for microbes and activates the classical pathway of the complement cascade.

The degree of pathogenicity.

They engulf and kill them innately.

Harmless bacteria consistently associated with the host.

5 days; they do not return to the blood and turn into pus.

IL-1, IL-6, and TNF-alpha.

Innate and Adaptive immune systems.

They present antigens bound to MHC-I or MHC-II on their cell surface.

They recognize patterns on foreign organisms and process/present antigens via MHC-II.

B-Lymphocytes.

Yes.

They present the antigen via MHC-II to T-Helper Cells, which then activate the B-Cell to differentiate into a Plasma Cell that secretes antibodies.

Non-specific; it responds to all foreign substances.

External barrier, innate immune response, and adaptive immune response.

They possess cytoplasmic granules and are named according to the staining ability of these granules. Eosinophils - Eosin dye. Basophils - Basic dyes

Systemic release of pro-inflammatory cytokines and pro-inflammatory complement, leading to vasodilation and septic shock.

To destroy infected or foreign cells, can be transferred from one individual to another via effector cells