immunity

• The innate immune system is genetically programmed, present from birth, and provides a rapid, non-specific response.

Lines of Defense

• The innate immune system includes physical and chemical barriers and cellular responses as the first and second lines of defense.

Adaptive Immune System

• The adaptive immune system is specific, responding to pathogens that evade the innate system.
• It has a lag phase upon initial exposure.
• It exhibits immunological memory, remembering primary responses for future threats.
• Self-tolerance is a feature of the adaptive immune system.

Humoral Response

• The humoral response targets pathogens in body fluids.
• B-cells, activated by Helper T cells, produce antibodies.
• Activated Helper T cells clone and differentiate.

Cell-Mediated Immunity

• Cell-mediated immunity targets intracellular pathogens.
• T-Lymphocytes are specialized white blood cells (WBCs) manufactured in bone marrow and matured in the thymus.
• T-Lymphocytes are stored in lymph nodes and lymphatic tissues like the spleen, thymus, tonsils, and liver.
• T-Lymphocytes possess surface receptor proteins that recognize specific antigens.

Types of T-Cells

• Helper T cells release chemicals activating cytotoxic T cells, B cells, and increasing macrophage activity post-antigen recognition.
• Cytotoxic T cells bind to and destroy infected cells.
• Memory T Cells remain in the body for secondary immune responses.
• Suppressor T Cells regulate the immune response.
• B-Lymphocytes are manufactured and mature in the bone marrow.
• After maturation, B cells migrate from bone marrow to lymph nodes and lymphatic tissue.
• They have surface antibody proteins specific to particular antigens

Antibodies

• Antibodies, also known as immunoglobulins, are proteins from plasma cells that attach to and destroy antigens.

Antibody Strategies

• Neutralization: Antibodies coat pathogens, blocking their activity.
• Agglutination: Neutralized pathogens clump together surrounded by thousands of antibodies.
• Precipitation of dissolved antigens.
• Activation of the complement system, leading to lysis of infected cells.
• Opsonization enhances phagocytosis.

Humoral Response

• B cells are activated when their surface antibodies bind to antigens, presenting them to Helper T cells.
• Activated Helper T cells release cytokines (interleukin-2) that activate B lymphocytes.
  • Activation leads to B cell multiplication with the same specificity.
  • B cell differentiate to plasma cells which secrete antibodies, and memory B cells which remain in lymphoid tissues.
• Plasma cells secrete antibodies that bind to the antigen, forming an antibody-antigen complex.
• Memory B cells are activated upon secondary exposure, leading to mitotic division and plasma cell formation.
• Somatic hypermutations result in more antibodies produced during secondary immune response.

Cell-Mediated Immunity Steps

• Macrophages engulf pathogens and display antigens via MHC II molecules.
• Antigen-presenting macrophages move to lymph nodes, activating matching Helper T cells.
• Activated Helper T cells differentiate into Cytotoxic T cells, Memory T cells & Suppressor T cells
• Cytotoxic T cells migrate to infection sites, bind to antigens on infected cells, and release cytokines to destroy them.
• Some cytotoxic cells produce interferons to protect healthy cells.
• Suppressor T cells regulate the immune response by ceasing the production and action of cytotoxic T cells once the infection has been defeated.
• Memory T cells remain, rapidly cloning upon re-exposure.

Primary Immune Response

• The body's initial immune response to an antigen.
• The body recognizes the antigen.
• The body induces a long-term memory response against the antigen.
• Antibodies are produced against the antigen.

Secondary Immune Response

• The immune system's reaction upon subsequent contact with an antigen.

Bacterial Innate Responses

• Complement proteins puncture bacterial cell walls, inducing lysis.
• Opsonized bacteria undergo phagocytosis.
• Neutrophil count increases.
• Monocytosis occurs.

Bacterial Adaptive Responses

• Antibody production by plasma cells.
• Cytokine production by T cells.
• Memory B cells formed.

Cholera Innate Response

• Production of cytokines and neutrophils in gut lining.
• Release of AMPs kill bacteria or induce inflammation.

Cholera Adaptive Response

• IgA secreted by gut lining protects from colonization, and increases the B lymphocytes specific to cholera antigens.
• B memory cells.

Fungal Innate Response

• Barriers such as the keratin layer of the skin prevent infections.
• Phagocytes bind to fungi.
• Neutrophil count increases.

Fungal Adaptive Response

• Dendritic cells transport fungi to lymph nodes, recruiting T cells.
• Heller T cells release cytokines to stimulate phagocytes.
• Keratinocytes express TLRs and defensins as a first-line response.
• The response to tinea is mediated by innate and adaptive (CMI) responses

Macroparasite Response

• Eosinophilia is shown via counts in response to bone marrow production of eosinophils.
• Cytokines → interleukins
• IgE levels in the peripheral blood increase.
• Eosinophils kill opsonized helminths.

Viral Innate Response

• Phagocytes detect cells with less MHCI receptors and kill them
• Dendritic cells recognize viral PAMPs and release interferons → activate adaptive immunity

Viral Adaptive Response

• Cytotoxic T cells recognize infected cells.
• Cytokines (interferon) prevent replication inside infected cells.
• Interferon signals neighboring cells to increase MHCI molecules.
• B lymphocytes produce antibodies, coating virus and preventing cell infection.
• Viruses also activate the complement system, damaging the viral envelope.

Protozoa Example (Malaria)

• Individuals are protected from the parasite due to changes in haemoglobin.
• Natural killer cells increase, causing lysis of infected red blood cells.
• Natural killer cells produce chemokines, which activate phagocytes.

Protozoa Adaptive Response

• Antibodies (IgM and IgG) are produced by plasma cells.
• Helper T cells control parasites.
• Antibodies inhibit merozoite invasion or enhance elimination of infected erythrocytes.
• Opsonization leads to increased phagocytosis, destruction by cytotoxic T cells, or parasite inhibition by neutrophils and macrophages.