Responsible for body defenses.
Nonspecific response (defense).
Examples: phagocytosis, inflammation.
Specific response (defense).
Production of specific antibodies against foreign substances.
Lymphoid structures.
Lymph nodes.
Spleen.
Tonsils.
Intestinal lymphoid tissue.
Lymphatic circulation.
Immune cells.
Lymphocytes.
Macrophages.
Tissues—immune cell development
Bone marrow
Origination of all immune cells
Thymus
Maturation of T lymphocytes
Chemical mediators
Histamine, interleukins
Antigens / Cells/ Complement System / Chemical Mediators
Antigens
Self
MHC is referred to as HLA (Human Leukocyte Antigen) proteins label cells of the individual.
Immune system ignores self-cells.
Non-self
Immune system recognizes specific nonself antigens as foreign.
Development of a specific response to that particular antigen
Memory cells produced to respond quickly to antigen
Usually exogenous substances
Cell surface antigens
Proteins
Polysaccharides
Glycoproteins
Macrophages (non specific)
Initiation of immune response
Develop from monocytes
Part of the mononuclear phagocytotic system
Engulf foreign material
Display antigens of foreign material
Secrete chemicals
Examples: monokines, interleukins
Present throughout the body
Lymphocytes ( one of the White Blood Cells)
There are 2 groups T and B Lymphocytes
T lymphocytes- Kills Directly
From bone marrow stem cells
Further differentiation in thymus
Cell-mediated immunity
Cytotoxic T killer cells
Helper T cells
Memory T cells
B lymphocytes- produce antibodies to kill
Responsible for production of antibodies
Humoral immunity
Mature in bone marrow
Proceed to spleen and lymphoid tissue
Plasma cells
Produce antibodies
B memory cells
Can quickly form clone of plasma cells
Humoral immunity: Antibodies are produced to protect the body. ( B cells)
Cell-mediated immunity (CMI): Lymphocytes are programmed to attack nonself cells to protect the body. ( T Cells)
IgG
Most common in blood comes from mother or after initial exposure ( IgM) – memory cells
IgM
First to increase in immune response – Initial exposure
IgA
In secretions
Tears
Saliva and mucous membranes
Colostrum
IgE
Allergic response
Causes release of histamine and other chemicals
Results in inflammation
IgD
Attached to B cells
Activates B cells
Activated during immune reactions with IgG or IgM
Group of inactive proteins circulating in blood
C1 to C9
Causes cell damage and further inflammation when activated
Involved in inflammation and immune reactions
Examples: histamine, cytokines
Variety of functions
Signaling
Causing cellular damage- can be self or pathogen
Self: like allergies
“self” antigen
Normally ignored by the immune system
Tolerance
“nonself” antigen
Foreign
Specific response to a specific antigen
Stored in memory cells for future reference
Natural immunity
Species-specific – things like distemper only animals can get like dogs
Innate immunity
Gene-specific
Related to ethnicity
Primary response
First exposure to antigen
1 to 2 weeks before antibody titer reaches efficacy
Secondary response
Repeat exposure to the same antigen
More rapid response, with efficacy in 1 to 3 days
Natural active
Mechanism: Pathogens enter body and cause illness; antibodies form in host
Memory: Yes
Example: Person has chickenpox once
Artificial active
Mechanism: Vaccine (live or attenuated organisms) is injected into person. No illness results, but antibodies form
Memory: Yes
Example: Person has measles vaccine and gains immunity
Natural passive
Mechanism: Antibodies passed directly from mother to child to provide temporary protection
Memory: No
Example: Placental passage during pregnancy or ingestion of breast milk
Artificial passive
Mechanism: Antibodies injected into person (antiserum) to provide temporary protection or minimize severity of infection
Memory: No
Example: Gammaglobulin if recent exposure to microbe
Some occurrence has declined where vaccination rates are high.
Previous infections
“herd immunity”
Outbreaks (measles, mumps) in North America due to inadequate revaccination of teens
Search for additional vaccines continuous
AIDS, malaria, tuberculosis and others
Research on genetic vaccines
Emerging infectious diseases
Newly identified in a population
Re-emerging infectious diseases
Previously under control
No consistence in vaccination programs
On rise due to globalization, drug resistance, and other factors
Example: measles in the United States
Biological agents used to attack civilians and/or military personal
May use altered antigenic forms of common viruses or bacteria
Widespread impact on population due to a lack of vaccines
Hyperacute rejection
Immediately after transplantation
Acute rejection
Develops after several weeks
Chronic, late rejection
Occurs after months or years
Reduction of immune response to prevent rejection
Commonly used drugs
Cyclosporine, azathioprine, prednisone
High risk of infection
Caused by immunosuppression
Opportunistic organisms
Type I hypersensitivity—allergic reactions (asthma/food allergy/anaphylaxis) - IgE
Common
Caused by allergen
Skin rashes
Hay fever
Causative mechanism
Exposure to allergen
Development of IgEs
Mast cells
Complications
Anaphylaxis
Type I hypersensitivity–allergic reactions (cont.)
Hay fever: allergic rhinitis
Nasal mucosa
Food allergies
Digestive tract mucosa
Atopic dermatitis/eczema
Skin
Asthma
Bronchial mucosa
Severe, life-threatening
Systemic hypersensitivity reaction
Decreased blood pressure caused by release of histamine
Airway obstruction
Severe hypoxia
Can be caused by:
Latex materials
Insect stings
Nuts or shellfish; various drugs
Signs and symptoms
Generalized itching or tingling, especially in oral cavity
Coughing / Difficulty breathing
Feeling of weakness / Dizziness or fainting
Sense of fear and panic
Edema around eyes, lips, tongue, hands, feet
Hives
Collapse with loss of consciousness
Antigen is present on cell membrane
May be normal body component or exogenous
Circulating IgGs react with antigen
Destruction by phagocytosis or cytolytic enzymes
Example
Response to incompatible blood transfusion
Graft Rejection
Know The Types of Graft: Xenograft / Alograft / Autograft
Antigen combines with antibody
Forms immune complexes, deposited in tissue
Activation of complement system
Process causes inflammation and tissue destruction
Examples:
Glomerulonephritis
Rheumatoid arthritis
SLE
Serum Sickness
Delayed response by sensitized T lymphocytes
Release of lymphokines
Inflammatory response
Destruction of the antigen
Examples
Poison Ivy
Tuberculin test
Contact dermatitis
Allergic skin rash
Development of antibodies against own cells or tissues
Autoantibodies are antibodies formed against self-antigens—loss of self-tolerance.
Disorder can affect single organs or tissues or can be generalized.
Examples:
Hashimoto thyroiditis, systemic lupus erythematosus, rheumatic fever, myasthenia gravis, scleroderma, pernicious anemia
Type III Hypersensitivity
Chronic inflammatory disease
Affects a number of organ systems
Characteristic facial rash—“butterfly rash”
Affects primarily young women
Incidence is higher in African Americans, Asians, Hispanics, Native Americans
Large number of circulating autoantibodies
Against DNA, platelets, erythrocytes
Formation of immune complexes
Deposited into tissues
Inflammation and necrosis
Vasculitis develops in many organs.
Impairs blood supply to the tissues
Signs and symptoms vary because of organ involvement but commonly include:
Arthralgia, fatigue, malaise
Cardiovascular problems
Polyuria
Partial or total loss of one or more immune system components
Predisposition to the development of opportunistic infections
Increased risk of infection and cancer
Primary deficiencies
Basic developmental failure somewhere in the system
Secondary or acquired immunodeficiencies
Loss of the immune response from specific causes
Can occur at any time during the life span
Infections, splenectomy, malnutrition, liver disease, immunosuppressant drugs, radiation, chemotherapy (cancer)
AIDS—chronic infectious disease caused by the human immunodeficiency virus (HIV)
HIV destroys helper T cells—CD4 lymphocytes.
Loss of immune response
Increased susceptibility to secondary infections and cancer
Prolonged latent period
HIV-positive individual
Virus is known to be in the body.
No evidence of immunosuppression
AIDS
Marked clinical symptoms, multiple complications
Individual often identified as HIV-positive before development of AIDS
Human immunodeficiency virus
Retrovirus
Member of the subfamily, lentavirus
HIV-1
Major cause of AIDS in US and Europe
HIV-2
Major cause of AIDS in central Africa
Bodily fluids
Blood
Semen
Vaginal fluids
Generalized effects
Lymphadenophathy
Fatigue and weakness
Headache
Arthralgia
Gastrointestinal effects primarily due to opportunistic infections
Encephalopathy
Sometimes called AIDS dementia
Direct infection of brain cells by HIV
Primary cause of death
Frequently multiple, more extensive and severe than usual
Lungs
Pneumocystis carinii
Herpes simplex
Cold sores
Candida
Involves mouth and often esophagus
Tuberculosis
Increased incidence of all cancers
Unusual cancers are often markers for AIDS.
Kaposi sarcoma
Affects the skin, mucous membranes, and internal organs
Non-Hodgkin lymphoma
Purple or brown nonpruritic, painless patches
Eventually become nodular
Responsible for body defenses.
Nonspecific response (defense):
This is the initial, rapid response to any foreign invader, regardless of its identity.
Examples:
Phagocytosis: Engulfing and destroying pathogens or debris by cells like macrophages and neutrophils.
Inflammation: A localized physical condition of redness, swelling, heat, and pain due to tissue damage or infection.
Specific response (defense):
This is a slower but more targeted response that involves the production of specific antibodies against foreign substances (antigens).
Key features:
Specificity: The immune response is tailored to the specific antigen encountered.
Memory: The immune system remembers previous encounters with antigens and can mount a faster and more effective response upon re-exposure.
Lymphoid structures:
These are the organs and tissues where immune cells develop, mature, and carry out their functions.
Lymph nodes:
Small, bean-shaped structures located along lymphatic vessels.
Filter lymph and contain lymphocytes and macrophages, which trap and destroy pathogens.
Spleen:
Located in the upper left abdomen.
Filters blood, removes damaged blood cells, and contains lymphocytes and macrophages that respond to bloodborne pathogens.
Tonsils:
Located in the throat.
Trap pathogens entering the body through the nose or mouth.
Intestinal lymphoid tissue (Peyer's patches):
Located in the lining of the small intestine.
Monitor the gut for pathogens and initiate immune responses.
Lymphatic circulation:
A network of vessels that collect and transport lymph, a fluid containing immune cells and antigens, throughout the body.
Immune cells:
These are the cells that carry out the immune response. Examples include:
Lymphocytes:
A type of white blood cell that includes T cells, B cells, and natural killer (NK) cells.
T cells and B cells are responsible for specific immunity, while NK cells are part of the innate immune system.
Macrophages:
Phagocytic cells that engulf and destroy pathogens, cellular debris, and foreign substances.
Also present antigens to T cells, initiating the adaptive immune response.
Tissues—immune cell development:
Bone marrow:
The soft, spongy tissue inside bones.
Site of origin of all immune cells.
Thymus:
Located in the chest.
Site of maturation of T lymphocytes (T cells).
Chemical mediators:
These are molecules that regulate the immune response. Examples include:
Histamine: A chemical released by mast cells during allergic reactions, causing inflammation and vasodilation.
Interleukins: A group of cytokines (signaling molecules) that regulate the growth, differentiation, and activation of immune cells.
Antigens / Cells / Complement System / Chemical Mediators
Antigens:
Substances that can trigger an immune response.
Self:
Molecules on the surface of an individual's cells that the immune system recognizes as "self".
MHC (major histocompatibility complex) is referred to as HLA (Human Leukocyte Antigen) proteins label cells of the individual.
Immune system ignores self-cells (self-tolerance).
Non-self:
Molecules on the surface of foreign cells, such as bacteria, viruses, fungi, and parasites, that the immune system recognizes as "foreign".
Immune system recognizes specific nonself antigens as foreign.
Development of a specific response to that particular antigen.
Memory cells produced to respond quickly to antigen.
Usually exogenous substances:
Cell surface antigens:
Proteins
Polysaccharides
Glycoproteins
Macrophages (non-specific):
Initiation of immune response
Develop from monocytes
Part of the mononuclear phagocytotic system
Engulf foreign material
Display antigens of foreign material
Secrete chemicals:
Examples: monokines, interleukins
Present throughout the body
Lymphocytes (one of the White Blood Cells):
There are 2 groups T and B Lymphocytes
T lymphocytes:
From bone marrow stem cells
Further differentiation in thymus
Cell-mediated immunity
Types:
Cytotoxic T killer cells: Directly kill infected cells or tumor cells.
Helper T cells: Secrete cytokines that activate other immune cells, including B cells and cytotoxic T cells (CD4+)
Memory T cells: Provide long-lasting immunity by remembering previous encounters with antigens.
B lymphocytes:
Responsible for production of antibodies
Humoral immunity
Mature in bone marrow
Proceed to spleen and lymphoid tissue
Plasma cells:
Produce antibodies
B memory cells:
Can quickly form clone of plasma cells
Humoral immunity: Antibodies are produced to protect the body. (B cells)
Cell-mediated immunity (CMI): Lymphocytes are programmed to attack nonself cells to protect the body. (T Cells)
IgG: Most common in blood, provides long-term immunity, can cross the placenta to protect the fetus; produced after initial exposure (IgM) – memory cells
IgM: First to increase in immune response, indicates acute infection – Initial exposure
IgA: Found in secretions, provides localized protection on mucous membranes in:
Tears
Saliva and mucous membranes
Colostrum
IgE: Involved in allergic response, binds to mast cells and basophils
Causes release of histamine and other chemicals
Results in inflammation
IgD: Attached to B cells, serves as a receptor
Activates B cells
Activated during immune reactions with IgG or IgM
Group of inactive proteins circulating in blood (C1 to C9)
Activation triggers a cascade of events that lead to:
Opsonization: Enhancing phagocytosis of antigens
Chemotaxis: Attracting immune cells to the site of infection
Cell lysis: Directly killing pathogens by disrupting their cell membranes
Causes cell damage and further inflammation when activated
Involved in inflammation and immune reactions
Examples: histamine, cytokines
Variety of functions:
Signaling
Causing cellular damage: can be self or pathogen
Self: like allergies
"self" antigen: Normally ignored by the immune system (tolerance)
"nonself" antigen: Foreign
Specific response to a specific antigen
Stored in memory cells for future reference
Natural immunity: Species-specific – things like distemper only animals can get like dogs
Innate immunity: Gene-specific, related to ethnicity
Primary response: First exposure to antigen, takes 1 to 2 weeks before antibody titer reaches efficacy
Secondary response: Repeat exposure to the same antigen, more rapid response, with efficacy in 1 to 3 days
Natural active:
Mechanism: Pathogens enter body and cause illness; antibodies form in host
Memory: Yes
Example: Person has chickenpox once
Artificial active:
Mechanism: Vaccine (live or attenuated organisms) is injected into person. No illness results, but antibodies form
Memory: Yes
Example: Person has measles vaccine and gains immunity
Natural passive:
Mechanism: Antibodies passed directly from mother to child to provide temporary protection
Memory: No
Example: Placental passage during pregnancy or ingestion of breast milk
Artificial passive:
Mechanism: Antibodies injected into person (antiserum) to provide temporary protection or minimize severity of infection
Memory: No
Example: Gammaglobulin if recent exposure to microbe
Some occurrence has declined where vaccination rates are high
Previous infections
“herd immunity”
Outbreaks (measles, mumps) in North America due to inadequate revaccination of teens
Search for additional vaccines continuous
AIDS, malaria, tuberculosis and others
Research on genetic vaccines
Emerging infectious diseases: Newly identified in a population
Re-emerging infectious diseases: Previously under control
No consistence in vaccination programs
On rise due to globalization, drug resistance, and other factors
Example: measles in the United States
Biological agents used to attack civilians and/or military personal
May use altered antigenic forms of common viruses or bacteria
Widespread impact on population due to a lack of vaccines
Hyperacute rejection: Immediately after transplantation
Acute rejection: Develops after several weeks
Chronic, late rejection: Occurs after months or years
Reduction of immune response to prevent rejection
Commonly used drugs: Cyclosporine, azathioprine, prednisone
High risk of infection caused by immunosuppression due to opportunistic organisms
Type I hypersensitivity—allergic reactions (asthma/food allergy/anaphylaxis)
IgE-mediated
Common
Caused by allergen
Skin rashes
Hay fever
Causative mechanism
Exposure to allergen
Development of IgEs
Mast cells
Complications
Anaphylaxis
Type I hypersensitivity–allergic reactions (cont.)
Hay fever: allergic rhinitis, affects nasal mucosa
Food allergies: affects digestive tract mucosa
Atopic dermatitis/eczema: affects skin
Asthma: affects bronchial mucosa
Severe, life-threatening systemic hypersensitivity reaction
Decreased blood pressure caused by release of histamine
Airway obstruction and severe hypoxia
Can be caused by:
Latex materials
Insect stings
Nuts or shellfish; various drugs
Signs and symptoms:
Generalized itching or tingling, especially in oral cavity
Coughing / Difficulty breathing
Feeling of weakness / Dizziness or fainting
Sense of fear and panic
Edema around eyes, lips, tongue, hands, feet
Hives
Collapse with loss of consciousness
Antigen is present on cell membrane
May be normal body component or exogenous
Circulating IgGs react with antigen
Destruction by phagocytosis or cytolytic enzymes
Example
Response to incompatible blood transfusion
Graft Rejection
Know The Types of Graft: Xenograft / Allograft / Autograft
Antigen combines with antibody, forming immune complexes, deposited in tissue
Activation of complement system
Process causes inflammation and tissue destruction
Examples:
Glomerulonephritis
Rheumatoid arthritis
SLE
Serum Sickness
Delayed response by sensitized T lymphocytes
Release of lymphokines, leading to inflammatory response
Destruction of the antigen
Examples:
Poison Ivy
Tuberculin test
Contact dermatitis
Allergic skin rash
Development of antibodies against own cells or tissues
Autoantibodies are antibodies formed against self-antigens—loss of self-tolerance.
Disorder can affect single organs or tissues or can be generalized.
Examples:
Hashimoto thyroiditis, systemic lupus erythematosus, rheumatic fever, myasthenia gravis, scleroderma, pernicious anemia
Type III Hypersensitivity
Chronic inflammatory disease affecting a number of organ systems
Characteristic facial rash—“butterfly rash”
Affects primarily young women, with higher incidence in African Americans, Asians, Hispanics, Native Americans
Large number of circulating autoantibodies against DNA, platelets, erythrocytes
Formation of immune complexes, deposited into tissues, leading to inflammation and necrosis
Vasculitis develops in many organs, impairing blood supply to the tissues
Signs and symptoms vary because of organ involvement but commonly include:
Arthralgia, fatigue, malaise
Cardiovascular problems
Polyuria
Partial or total loss of one or more immune system components
Predisposition to the development of opportunistic infections and increased risk of infection and cancer
Primary deficiencies: Basic developmental failure somewhere in the system
Secondary or acquired immunodeficiencies: Loss of the immune response from specific causes, can occur at any time during the life span
Infections, splenectomy, malnutrition, liver disease, immunosuppressant drugs, radiation, chemotherapy (cancer)
AIDS—chronic infectious disease caused by the human immunodeficiency virus (HIV)
HIV destroys helper T cells—CD4 lymphocytes, leading to loss of immune response
Increased susceptibility to secondary infections and cancer
Prolonged latent period
HIV-positive individual: Virus is known to be in the body but with no evidence of immunosuppression
AIDS: Marked clinical symptoms, multiple complications
Individual often identified as HIV-positive before development of AIDS
Human immunodeficiency virus (HIV)
Retrovirus, member of the subfamily lentavirus
HIV-1: Major cause of AIDS in US and Europe
HIV-2: Major cause of AIDS in central Africa
Bodily fluids:
Blood
Semen
Vaginal fluids
Generalized effects:
Lymphadenophathy
Fatigue and weakness
Headache
Arthralgia
Gastrointestinal effects primarily due to opportunistic infections
Encephalopathy: Sometimes called AIDS dementia due to direct infection of brain cells by HIV
Primary cause of death
Frequently multiple, more extensive and severe than usual
Lungs: Pneumocystis carinii
Herpes simplex: Cold sores
Candida: Involves mouth and often esophagus
Tuberculosis
Increased incidence of all cancers
Unusual cancers are often markers for AIDS:
Kaposi sarcoma: Affects the skin, mucous membranes, and internal organs
Non-Hodgkin lymphoma: Purple or brown nonpruritic, painless patches that eventually become nodular