IMM1: Introduction to Immunology and innate immunity
Immune system
Our immune system ensures that we stay healthy. It is a diffuse, complex network of interacting cells,
cell products, and cell-forming tissues that protect the body. The immune system defends the body
against pathogens and other foreign substances, destroys infected cells, and removes cellular debris.
The immune system distinguishes between self and non-self, as well as between harmful and
harmless substances. There is a balance between activation (inflammation) and inhibition
(tolerance). An imbalance in immunity can lead to certain diseases.
Part I: Immune system and defense
First line of Defense: Physical Barrier
The physical barrier forms the first line of defense against pathogens.
Second line of Defense: Innate Immune system (Non-specific)
The innate immune system acts as the second line of
defense. It responds quickly, does not adapt or change,
has limited recognition ability, and remains constant
throughout an infection.
This system includes granulocytes (neutrophils),
monocytes, macrophages, NK cells, and dendritic cells.
Cytokines signal to other cells to act, sometimes
instructing cells to deactivate instead of activating. Chemokines signal cells to move to a specific
location, guiding them on where to go and when to stop.
Third line of defense: adaptive immune system (specific)
The adaptive immune system forms the third line of
defense. Unlike the innate system, the adaptive immune
system responds slowly, has the ability to change,
recognizes pathogens more effectively, and improves
during an infection.
This system utilizes B cells and T cells and leads to the
production of antibodies.
1. Primary Response: In this initial response, the adaptive immune cells form after the first
contact with an antigen. B cells are produced in the bone marrow, and T cells in the
thymus. The primary response occurs slowly because the antigen has not yet been
recognized.
2. Secondary Response: Upon subsequent contact with the same antigen, previously
formed adaptive immune cells are quickly activated. This secondary response is rapid
because the antigen is already recognized. This activation occurs in the lymph
nodes, spleen, and GALT (gut-associated lymphoid tissue).
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, The Cooperation Between the Innate and Adaptive Immune Systems Is Crucial for Effective Pathogen
Control. This Happens in Two Ways:
1. Activation of the Adaptive Immune System:
Innate dendritic cells capture pathogens and
present antigens to T cells in the lymph nodes,
stimulating a specific immune response and
thereby activating the adaptive immune system.
2. Activation of Innate Immune Cells: T cells and
antibodies from the adaptive immune system
activate innate immune cells, such as
macrophages and neutrophils. T cells release
signals that activate these cells, while antibodies help
in recognizing and eliminating pathogens.
Hematopoiesis is the process of immune cell development. There are two common precursor cells:
1. Lymphoid Progenitor Cells: These develop into lymphocytes, which belong to the adaptive
immune system (except for NK cells).
2. Myeloid Progenitor Cells: These develop into myeloid cells, which are part of the innate
immune system.
Part II: complement system
Complement system
The Complement System Plays a Key Role During Inflammation Caused by Bacterial Infections
Your complement system supports sustained inflammation and consists of plasma proteins with
enzymatic activity.
The complement system is an essential part of the immune system, with the most significant factor
being C3. When C3 is activated, it undergoes a cleavage reaction that allows it to mark pathogens
and attract immune cells. This cleavage produces two fragments: C3a and C3b because of an
enzymatic reaction. C3 only becomes active after being split into C3a and C3b.
C3a functions as an anaphylatoxin, meaning it attracts immune cells to the infection site and
promotes inflammatory responses. C3b, on the other hand, enables complement fixation by binding
to pathogens. This marks the pathogens for phagocytosis, a process in which immune cells ingest and
destroy pathogens. Additionally, C3b can contribute to lysis, the breakdown of the bacterial cell wall.
These mechanisms ultimately lead to the phagocytosis and destruction of pathogens, allowing the
body to effectively respond to infections.
Complement Fixation refers to the process by which C3b binds to pathogens, enhancing
phagocytosis. When immune cells, such as phagocytes, are attracted, they express complement
receptors (CR) that efficiently bind to C3b-coated pathogens. This binding stimulates the uptake of
pathogens by phagocytes through endocytosis or phagocytosis. The ingested pathogens are then
broken down by fusion with acidic lysosomes within the phagocyte, where enzymes destroy the
pathogens.
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