[PHY LEC - LE 2] 03 - WBC and Intro to Immunology_ Ver. 1.0

<1%.

Resident phagocytic cells.

They are populated by commensal organisms, contain innate and adaptive immune cells, and include mechanical and chemical barriers.

Antagonism refers to one cytokine counteracting or inhibiting the actions of another cytokine.

To function as antigen presenting cells and link the innate and adaptive immune responses.

It traps microbial particles, which are then removed by cilia movement, coughing, or sneezing.

They recognize and respond to common microbial structures.

It is associated with mucosal tissues and initiates immune responses to specific antigens.

Through mucosal surfaces or breaches in the skin.

IL-10 and TGFβ (Transforming Growth Factor Beta).

Over 400 square meters.

C3b attaches to the surface of pathogens, tagging them for destruction and enhancing phagocytosis.

They have pink-staining cytoplasmic granules.

Washing action of tears, saliva, and urine, along with secreted body fluids that have bactericidal components.

Pro-inflammatory and anti-inflammatory cytokines.

Regulation of immune response.

WBCs are crucial for immune response, including fighting infections and regulating inflammation.

1-3%.

Plasmacytoid dendritic cells and virus-infected cells.

They release inflammatory mediators and are involved in allergic reactions.

Acute-phase responses.

IL-12 and IL-18.

Cytokines can produce similar effects and can stimulate the production of additional cytokines, creating a cascade effect.

Tight junctions, keratin, and mucus assisted by cilia and peristalsis.

Endogenous molecules produced by or released from damaged or dying cells.

Proteins whose concentration is increased or decreased by at least 25% following injury.

CRP is a non-specific marker of inflammation used to monitor or detect significant inflammation in acute conditions.

It helps in diagnosing and treating various immune-related conditions and diseases.

Skin barriers are external, while mucosal barriers are found in respiratory, gastrointestinal, and genitourinary tracts.

They migrate out of the lymph node and join the bloodstream.

Complements, cytokines, and chemokines made by specific cells.

The end product of the complement cascade that creates pores in target pathogens' cell membranes.

Innate immunity is non-specific and immediate, while adaptive immunity is specific and develops over time.

IFN α and IFN β, which mediate the early innate immune response to viral infections.

The phases include recognition, activation, and effector phases.

IL-1, IL-6, and TNF-α (Tumor Necrosis Factor Alpha).

Fc receptors, TLR, receptors for IL-5 and IL-3.

Peyer patches in the small intestine and isolated lymphoid follicles.

Molecular structures produced by microbial pathogens essential for their survival.

Through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs).

Antimicrobial compounds and cytokines.

Certain inflammatory diseases present with characteristic cytokine profiles, and balancing them is crucial for treatment.

They compete effectively against many potential pathogens.

Proteins produced as a systemic response to injury.

Classical, alternative, and lectin pathways.

The classical pathway is initiated by antigen-antibody complexes, while the alternative pathway is activated by direct contact with pathogens.

Pleiotropy, synergy, and redundancy.

C5 convertase in the form C4b2a3b.

It involves neutrophil activation, granule lysis, and the release of DNA and granule contents to immobilize and kill extracellular microbes.

C3b serves as the binding site for C5 serum protein, which is split into C5a and C5b.

Hematopoiesis.

Through breaches in the skin or mucosal surfaces.

They offer promise for treating viral infections, immunodeficiencies, autoimmune diseases, some cancers, and transplant rejection.

Type I interferon.

They are produced by neutrophils and barrier epithelial cells to provide direct toxicity to microorganisms.

Phagocytes and dendritic cells.

C3b functions as an opsonin, coating organisms for eventual killing by phagocytes.

After more than 96 hours.

Serum amyloid A can rise a thousand-fold during inflammation and helps recruit immune cells to the inflammation site.

They are granulocytic cells important in the body's defense against parasitic organisms.

Basophils, eosinophils, and neutrophils, characterized by their cytoplasmic granules.

They do not express antigen-specific receptors.

The process by which antigen-presenting cells display antigens on their surface to T cells.

Innate immunity is rapid and nonspecific, while adaptive immunity is slow, specific, and has memory.

Induces acute phase responses.

In secondary lymphoid structures, such as lymph nodes.

They bind to microbes to enhance phagocytosis and promote inflammatory responses.

The activation of innate immune cells by microbes leads to the release of pro-inflammatory cytokines.

They capture microbial antigens that enter the skin, gastrointestinal tract, and respiratory tract.

Immune cells are able to recognize them right away.

Within 0-4 hours.

They kill tumor cells and infected cells that lack MHC Class I expression.

Pluripotent hematopoietic stem cells in the bone marrow.

They are expert phagocytes and professional antigen-presenting cells.

They communicate signals, instruct cells to proliferate, differentiate, secrete additional cytokines, migrate, or die.

Inflammation, enhanced adaptive immunity, killing of microbes, tissue repair, and homeostasis.

T cells are primarily involved in cell-mediated immunity, while B cells are responsible for humoral immunity and antibody production.

Immunity is the ability to protect oneself from disease.

IL-1, IL-6, TNFα (Tumor Necrosis Factor Alpha).

Cytokines are chemical mediators produced by T cells, innate lymphoid cells, and mononuclear phagocytes.

They take up residence in various locations in the body.

Susceptibility to opportunistic infections, such as Candida and Clostridium, may increase.

Receptors used by innate immunity to recognize PAMPs and DAMPs.

Classical Pathway, Mannose Binding Lectin Pathway, and Alternative Pathway.

They recognize PAMPs and activate signal transduction pathways.

C3a acts as a chemoattractant for eosinophils, while C5a acts as a chemotactic agent for neutrophils and monocytes.

C3a and C5a are anaphylatoxins that trigger degradation of mast cells and basophils, releasing histamine and enhancing vascular permeability.

Lysozyme, collagenase, elastase, myeloperoxidase, defensins, and cathelicidin.

They capture, process, and present antigens to T cells, activating them.

The main types include IgG, IgA, IgM, IgE, and IgD, each with distinct functions.

To protect the body from pathogens and maintain homeostasis.

Primary organs include the bone marrow and thymus; secondary organs include lymph nodes and spleen.

By inhibiting protein synthesis, degrading viral RNA, and inhibiting viral gene expression and assembly.

Antimicrobial chemicals produced by epithelial cells of mucosal surfaces and granule-containing leukocytes.

Over 50 serum glycoproteins that cooperate with both the innate and adaptive immune systems.

Direct microbial killing, opsonization, activation of inflammatory response, cellular activation for microbial killing, and clearing immune complexes.

By immune complexes that recognize preformed IgM or IgG Ag-Ab complexes.

CD55 (Decay Accelerating Factor) and CD59 (Membrane Inhibitor of Reactive Lysis).

They both express high-affinity plasma membrane receptors for IgE.

Myeloid progenitor and lymphoid progenitor.

Cytokines bind with high affinity to receptors and utilize the JAK-STAT signaling pathway.

Interleukins and other cytokines such as stem cell factors, GCSF, and GM-CSF.

Dendritic cells (conventional), neutrophils, basophils, and macrophages.

Class I MHC presents endogenous antigens to CD8+ T cells, while class II MHC presents exogenous antigens to CD4+ T cells.

Leukocytes are involved in phagocytosis, inflammation, and adaptive immune responses.

APCs process and present antigens to T cells, initiating the adaptive immune response.

Cytokines are signaling molecules that mediate and regulate immunity, inflammation, and hematopoiesis.

A transient increase in the number of circulating white blood cells during acute infection.

NK cells, macrophages, and mast cells.

Phagocytic cells of the central nervous system.

Hematopoietic stem cells (HSCs).

Recognition and elimination of pathogens, and development of immune cells.

The immune system may recognize transplanted tissues as foreign and mount a response against them.

They mature and transport the antigens to regional lymph nodes.

They are innate lymphoid cells that do not express antigen-specific receptors.

They have blue-staining cytoplasmic granules.

High levels of peptide-MHC complexes, host stimulators, and cytokines.

Leukocytosis is the increased release of neutrophils and monocytes from the bone marrow, promoted by cytokines.

Lymphokines, monokines, chemokines, interleukines, and interferons.

Phagocytic macrophages or dendritic cells.

It involves T lymphocytes that directly attack infected or cancerous cells.

B cells differentiate into plasma cells that produce antibodies in response to antigens.

IgG provides long-term immunity, IgA protects mucosal surfaces, IgM is the first antibody produced, IgE is involved in allergic reactions, and IgD is a receptor on B cells.

Levels of defense include physical barriers, innate immune response, and adaptive immune response.

Granulocytes (neutrophils, eosinophils, basophils, mast cells), monocytes, and macrophages.

They are the principal cell type in acute inflammatory reactions and function as phagocytic cells.

They initiate protective responses against viruses involving helper T-cells and cytotoxic T-cells.

Activation occurs when C3 levels in the serum become low.

A structure formed by C5b and complementary proteins that can insert into the membrane of target cells, leading to cell lysis.

Dendritic cells, neutrophils, NK cells, basophils, macrophages, and ILCs.

The phases include activation of B cells, clonal expansion, and differentiation into plasma cells that produce antibodies.

The immune system can cause prolonged inflammation, which may lead to tissue damage and disease.

Leukocytosis, increased synthesis of ACTH and hydrocortisone, induction of fever, and initiation of adaptive immune response.

Fever is caused by the hypothalamus responding to elevated levels of acute phase proteins, influenced by TNF and IL-1.

T cells and B cells.

Cytokines are structurally diverse polypeptides that function as messenger molecules in the immune system.

They promote inflammation.

CD4+ T helper cells assist other immune cells, while CD8+ cytotoxic T cells kill infected or cancerous cells.

The immune system can overreact to harmless substances, leading to allergic reactions.

They are dendritic cells involved in T-helper mediated immunity against skin pathogens.

Complexes between bacterial mannose residues and plasma protein lectin.

5-12 days.

Histamine and various pharmacologically active substances.

Tissue-resident macrophages that usually arise early in life from embryonic cells.

They are soluble components present in plasma, primarily made by the liver.

T cells and B cells.

B cells can be activated through T-dependent and T-independent pathways.

Immunology is the study of cells, organs, and molecules responsible for immunity and their interactions.

About 7,000 leukocytes.

Inflammatory monocytes and patrolling monocytes.

Recognizing microbial molecules and host molecules produced in response to infections or injury.

The immune system mistakenly attacks the body's own tissues, leading to autoimmune conditions.

It is triggered by contact with viruses, bacteria, fungi, and tumor cells, independent of Ag-Ab interactions.

The myeloid lineage, including erythrocytes, megakaryocytes, and leukocytes.

PRRs, including TLR, cytokine receptors, and complement receptors.

Immunodeficiency results in a weakened immune response, increasing susceptibility to infections.

T cell activation requires recognition of the antigen-MHC complex and co-stimulatory signals from antigen presenting cells.

The primary response is slower and occurs upon first exposure to an antigen, while the secondary response is faster and stronger due to memory cells.