Types of immunity

Classification of immunity

Immunity is classified into innate immunity and specific or adaptive immunity

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- Innate immunity provides nonspecific defenses present from birth

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while adaptive immunity targets specific antigens and develops immunological memory.

Innate immunity: characteristics and defenses

-Innate immunity is present from birth and responds rapidly to foreign substances without requiring previous exposure

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Defenses:

-Its first line of defense consists of external barriers

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-while its second line includes phagocytes natural killer cells inflammation and complement, interferons

Specific or adaptive immunity: characteristics

Adaptive immunity

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-responds to specific antigens

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- has specificity systemic activity

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-memory B and T lymphocytes are its main cells and subsequent exposure to the same antigen can produce a faster stronger response.

Immune system: major components

-The hematopoietic system which produces blood cells

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-the vasculature which transports immune cells and

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-the lymphatic system which supports immune surveillance and transport.

Antigens and immunogens

Antigens are molecules recognized by the immune system that can initiate a specific immune response.

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An immunogen is a substance that actually induces an immune response and is therefore the more precise term for an immune-response-triggering substance.

Antibodies: definition and function

Antibodies also called immunoglobulins or gamma globulins are Y-shaped proteins produced by plasma cells.

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- They bind specific antigens and help neutralize them or promote their removal.

Intracellular versus extracellular pathogens

Intracellular pathogens enter host cells to reproduce such as viruses while extracellular pathogens remain outside host cells.

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-Cell-mediated immunity is especially important against intracellular pathogens whereas antibodies and phagocytes are important against many extracellular pathogens.

Innate surface defenses: skin and mucous membranes(bK)

Glycocalyx and recognition of self versus non-self

The glycocalyx is the carbohydrate-rich coating on cell surfaces. Recognition of surface molecules helps innate defenses distinguish many normal body cells from foreign material.

Macrophages: origin and general functions

Macrophages develop from monocytes and engulf pathogens foreign material and cellular debris.

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They also help coordinate immune responses and can present antigen fragments to T cells.

Free versus fixed macrophages(bk)

Free macrophages move through tissues to locate and engulf foreign material while fixed macrophages remain associated with particular tissues.

Examples of fixed macrophages include Kupffer cells in the liver and microglia in the brain.

Neutrophils eosinophils and mast cells

Neutrophils rapidly respond to infection and ingest pathogens;

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eosinophils attack parasites mainly by releasing substances from granules and also participate in allergic reactions;

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mast cells release inflammatory substances and help coordinate inflammation.

Phagocytosis mechanism(bk)

Phagocytosis: adherence and opsonization

Adherence occurs when a phagocyte attaches to a pathogen. Opsonization coats the pathogen with substances such as complement proteins or antibodies making it easier for phagocytes to recognize and bind.

Phagocytosis: ingestion and phagolysosome formation

During ingestion a phagocyte surrounds the pathogen and encloses it in a phagosome. The phagosome fuses with a lysosome to form a phagolysosome where digestive substances help break down the pathogen.

Respiratory burst defensins and enzymatic digestion

A respiratory burst produces reactive oxygen substances that help kill engulfed microbes; defensins are antimicrobial proteins that damage pathogen membranes; digestive enzymes break pathogens into smaller components.

Natural killer cells: characteristics and mechanism

Natural killer cells are large granular lymphocytes that attack certain virus-infected and abnormal cells without the antigen-specific recognition used by cytotoxic T cells

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They release perforins that form pores in target-cell membranes and chemicals that can enhance inflammation.

Inflammation: triggers and beneficial effects

Inflammation is a localized tissue response to injury, infection, heat trauma or chemical irritation

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-It helps prevent the spread of injury

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- remove pathogens and cellular debris and

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- promote tissue repair.

Cardinal signs of inflammation

The cardinal signs are redness

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-Redness: Increased blood flow causes redness

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-Heat: Denature proteins or vital enzymes

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-Swelling:heat fluid accumulation

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-Pain: chemicals released by mast cells stimulate local sensory neurons resulting in pain

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-Functional impairment / rigor

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Inflammation mechanism

Function of Mast cells in inflammation

mast cells release histamine, heparin, prostaglandins, and other chemicals into interstitial fluid. The histamine makes capillaries more permeable and increases blood flow through the area.

Explain Phagocytic Mobilization: in inflammation

Phagocytic Mobilization:

How the body recruits white blood cells (neutrophils) to site of injury or infection

* 1. Neutrophils enter blood from bone marrow:

Neutrophils are produced in the bone marrow and released into the bloodstream, ready to be deployed to sites of tissue damage

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* 2. Margination: As blood flow slows down in the capillaries near the inflamed site, neutrophils cling to the inner walls (endothelium) of the blood vessels

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* 3. Diapedesis: Chemical signals prompt the neutrophils to flatten out and squeeze through the gaps between the endothelial cells of the capillary wall to enter the surrounding tissue

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* 4. Positive Chemotaxis: Inflammatory chemicals released at the injured site act as chemotactic agents, creating a chemical trail that guides the neutrophils directly to the source of the damage or infection.

Function of Neutorphils in inflammation

Neutrophils are drawn to the area by chemotaxis, where they attack cellular debris (organic waste from dead cells) and bacteria.

(1) they stick to the side of the vessel and move into the tissue by emigration;

(2) their metabolic rate goes up dramatically, and while this respiratory burst continues, they generate reactive compounds, such as nitric oxide and hydrogen peroxide, that can destroy engulfed pathogens; and

(3) they secrete cytokines that attract other neutrophils and macrophages to the area

Leukocytosis and margination

Leukocytosis is an increase in circulating white blood cells supported by their release from bone marrow during inflammation.

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-Margination occurs when white blood cells move toward vessel walls as blood flow changes.

Pavementing diapedesis and chemotaxis

Pavementing or adhesion occurs when white blood cells attach to the endothelial lining of blood vessels;

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diapedesis is their passage through vessel walls into tissues;

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chemotaxis is their movement toward chemical signals released at the site of injury or infection.

Neutrophils monocytes and macrophages during inflammation

Neutrophils usually arrive early and attack pathogens.

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Monocytes subsequently enter tissues and develop into macrophages which remove pathogens and cellular debris and may predominate during chronic inflammation.

Complement system: definition and activation

Complement is a group of plasma proteins that activate one another in a cascade in the presence of foreign substances

Complement system: major functions

- enhances inflammation

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- coats pathogens to improve phagocytosis

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- form a membrane attack complex that damages susceptible target-cell membranes

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It therefore strengthens both innate and adaptive immune defenses.

Adaptive immunity

Specific:

means targeting particular antigens

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- systemic: Adaptive defenses are not restricted to the original infection site

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- memory:

means subsequent exposure to the same antigen can produce a faster more vigorous response.

Humoral versus cell-mediated immunity

Humoral immunity

- involves B cells plasma cells and antibodies

-important against many extracellular pathogens

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- cell-mediated immunity primarily

- involves T cells and their actions

-is particularly important against infected or abnormal cells.

overview of humoral response bk

clonal selection

Clonal selection occurs when an antigen binds to a matching B-cell receptor and selects that B cell for activation

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-The selected cell multiplies to produce a clone of antigen-specific cells that can differentiate into plasma cells and memory B cells.

Clonal selection explain

1. Primary Response (Initial Encounter)
-Antigen Binding: When antigens enter the body, they bind only to the specific B lymphocytes that have complementary receptors; B cells with non-complementary receptors remain inactive

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Proliferation: The activated B cell enlarges into a B lymphoblast and undergoes rapid division to form a clone of identical cells.

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*Differentiation: The cloned cells differentiate into two main types:
* Plasma cells: Active factories that secrete massive amounts of antibody molecules to neutralize the current threat.
* Memory B cells: Long-lived cells that "remember" the specific antigen for future protection

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2. Secondary Response (Subsequent Encounter)
Re-exposure: If the exact same antigen enters the body years later, the long-lived memory B cells recognize it immediately.
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Rapid Amplification: The secondary challenge triggers a much faster and significantly larger clone response compared to the primary response

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*Amplified Output: This results in a massive generation of plasma cells quickly producing a high volume of secreted antibodies, alongside the creation of even more memory B cells.

Active immunity: definition and mechanism

Active immunity develops when a person's own immune system responds to an antigen and produces an immune response.

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- It can generate memory cells and is generally longer-lasting than passive immunity although duration varies.

Naturally versus artificially acquired active immunity

Naturally acquired active immunity develops following natural exposure such as infection while artificially acquired active immunity develops following vaccination. Both stimulate the person's own immune system and can produce immune memory.

Vaccines and booster doses

Vaccines expose the immune system to an antigen or an appropriate representation of it and stimulate a primary immune response without requiring the person to undergo the intended disease. Booster doses re-expose the immune system to the antigen and can strengthen immune memory and protection.

Passive immunity: definition and mechanism

Passive immunity occurs when antibodies are received from another source rather than produced through the recipient's own primary response

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. It provides rapid but temporary protection because the transferred antibodies gradually break down and normally do not establish immune memory.

Naturally versus artificially acquired passive immunity

Naturally acquired passive immunity includes maternal IgG antibodies crossing the placenta and providing temporary protection to the baby while breast milk supplies antibodies such as IgA.

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Artificially acquired passive immunity involves administered antibody preparations such as certain antitoxins antivenoms and immunoglobulins.

Active versus passive immunity

Active immunity involves the person's own response and can create immune memory but usually takes time to develop

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. Passive immunity provides antibodies directly and acts rapidly but protection is temporary and does not normally create memory.

Antibody structure: variable hypervariable and constant regions

The variable region helps determine which antigen an antibody binds; the hypervariable region forms key contacts with the antigen; the constant region determines the antibody class and influences interactions with immune cells and complement.

Five antibody classes and their functions

IgM is usually the first antibody class produced in a primary response; IgG provides important systemic protection and crosses the placenta; IgA protects mucosal surfaces and occurs in secretions; IgD functions mainly as a receptor on naive B cells; IgE participates in allergic reactions and defense against certain parasites.

Antigen-antibody complex formation

An immune complex forms when an antibody binds to its matching antigen. This binding can neutralize harmful substances promote pathogen removal or initiate complement activation and other immune mechanisms.

Antibody action: complement fixation and neutralization

Complement fixation activates the complement cascade after appropriate antigen-antibody binding helping promote inflammation and destruction of susceptible targets. Neutralization occurs when antibodies bind pathogens or toxins and prevent them from attaching to or entering cells.

Antibody action: agglutination and precipitation

Agglutination occurs when antibodies bind multiple cells or particles together into clumps; precipitation occurs when antibodies bind soluble antigens and form complexes that can become insoluble and easier to clear.

Antibodies: inflammation and phagocytosis

Antibodies can coat pathogens and help phagocytes recognize and engulf them. Antigen-antibody complexes can also activate complement and promote inflammatory responses.

Antigen-presenting cells: function and examples

Antigen-presenting cells take up foreign material process it into antigen fragments and display those fragments on their surface for T-cell recognition. Macrophages and B lymphocytes can act as antigen-presenting cells.

Major histocompatibility complex (MHC)

MHC molecules display antigen fragments on cell surfaces so T cells can recognize them. MHC class I is found on almost all nucleated body cells while MHC class II is found mainly on professional antigen-presenting cells.

MHC class I and endogenous antigens

MHC class I mainly displays fragments of proteins produced inside a cell including viral proteins in infected cells

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These fragments can be recognized by CD8 cytotoxic T cells which may destroy the infected or abnormal cell.

MHC class II and exogenous antigens

MHC class II mainly displays fragments of material taken up from outside the cell and processed by antigen-presenting cells. These fragments are recognized by CD4 helper T cells which coordinate immune responses.

CD4 helper T cells: major functions

Helper T cells release cytokines and provide signals that activate B cells to produce antibodies stimulate cytotoxic T cells and help macrophages destroy ingested microbes. They coordinate and amplify adaptive immune responses.

TH1 and TH2 helper T-cell subtypes

TH1 cells mainly support defenses against intracellular pathogens by activating macrophages and promoting cytotoxic T-cell responses. TH2 cells mainly support responses against extracellular parasites and other appropriate targets by helping stimulate B cells and antibody production.

Cytotoxic T cells: recognition and activation

Cytotoxic T cells recognize specific antigen fragments displayed on MHC class I of target cells. Helper T-cell signals can assist their activation and expansion allowing them to target infected or abnormal cells.

Cytotoxic T cells: perforin and granzymes

Cytotoxic T cells release perforin which helps form pores in the target-cell membrane and granzymes which enter and activate processes that cause the target cell to die. The cytotoxic T cell can then detach and move on to another target.

Regulatory T cells

Regulatory T cells release inhibitory signals that reduce excessive B-cell and T-cell activity. They help maintain self-tolerance and reduce the risk of autoimmune responses.

Gamma-delta T cells

Gamma-delta T cells are a distinct T-cell group found in tissues including the intestinal lining. They help monitor for threats and respond to infection or tissue changes.

Primary immune response

The primary immune response occurs when the body encounters a particular antigen for the first time. Specific lymphocytes must be activated and multiply so the response develops more slowly and memory B and T cells may form.

Secondary immune response

The secondary immune response occurs when the body encounters the same antigen again. Memory lymphocytes respond more rapidly and usually produce a stronger response than during the primary exposure.

Primary versus secondary immune response

The primary response is generally slower because antigen-specific cells must first be activated and expanded; the secondary response is faster and stronger because memory cells already exist. Booster vaccinations use this principle to strengthen protection.

Primary immunodeficiency

Primary immunodeficiency usually results from inherited or genetic defects affecting components such as B cells T cells phagocytes or complement. The affected component determines which immune functions are weakened.

Secondary immunodeficiency

Secondary immunodeficiency develops because of another condition or external factor such as infection malnutrition aging or medications including chemotherapy glucocorticoids and some immunosuppressive drugs.

Immunosuppression: meaning and consequences

Immunosuppression is the reduction of immune-system activity and may be medically necessary such as after organ transplantation. However reduced immune activity can also increase susceptibility to infections.