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White blood cells
Organisation of the Body
| Question | Answer |
|---|---|
| Physiological challenges | Do no harm when all is normal Defend rapidly against pathogens Keep defending against persistent pathogens Eliminate self cells that are abnormal Keep a rapid response memory of previously encountered pathogens |
| White cells | <0.2% of blood cells are white 7000 per ul of blood All are CD45+ |
| Types of white blood cell | Neutrophils - 62% Lymphocyte - 30% Monocyte - 5% Eosinophils - 2.5% Basophils - 0.75% |
| Fractionation of white blood cells | Tube contains heparin to prevent clotting Spun in a centrifuge Lymphoprep splits cells due to high molecular weight Granulocytes bind to lymphoprep and aggregate so move downwards All other wbcs form a thin layer of monocyte cells |
| Quantifying leukocyte subsets by flow cytometry | Draw blood from subject Separate mononuclear cells using a ficoll gradient Stain with fluorescent antibody conjugates Optimise fluorescence detector sensitivity Pass stained cell suspension through laser beam Gate cell populations of interest |
| Origins of white cells in haematopoiesis | Come from haematopoietic stem cells Antigens are characteristic of each cell type, changing during differentiation All are CD7- |
| Granulocytes | CD15+ phagocytic cells that have specialised lysosomes |
| Neutrophils - polymorphonuclear cells | Phagocytes - modified endocytosis Receptors recognise proteins repeating patterns Dynein used to enclose membrane around pathogen Contains granules e.g. azurophilic |
| Mobility of neutrophils | 1 - respond to chemotactic chemicals e.g. pathogen products and chemokines 2 - adhere to endothelium by low affinity to GAGs and high affinity to ICAM-1 3 - extravasate by breaking down endothelium to enter tissues 4 - kill pathogen and die |
| Eosinophils | Larger than neutrophils Granules cationic - eosinophilic Stain orange pink in eosin due to eosinophil catatonic protein and peroxidases Recruited by T lymphocytes Receptors for IgE antibody Defence against parasites Host damage in allergies + asthma |
| Basophils | Least common leukocyte type Stain with basic dyes Granules contain heparin and histamine Similar to mast cells in tissues Rapidly produce interleukins IL4 and IL13 on activation |
| Monocytes | 5-10% of leukocytes Nucleus often kidney shaped no obvious granules CD14+ Precursor of macrophages in inflamed tissues Not blood cells - macrophages |
| Lymphocytes | Antigen specific, genetic innovators Can proliferate when stimulated Leave blood and enter lymph nodes via High Endothelial Venules Can rearrange their genome - different genes to allow recognition of different antigens |
| Lymphoid anatomy | All lymphocytes arise from haematopoiesis in bone marrow T cell mature in the thymus Lymphocytes encounter antigens in secondary lymphoid organs e.g. lymph nodes, spleen and peyers patches Immune reactions generate more lymphocytes |
| Natural killer cells | Some scattered cytoplasmic granules Defence against renegade cells Patrols body for missing self - absence of cell surface passport molecules Kills suspect cells by secreting toxins Important for fetus to survive as an allograph |
| B cells | CD19+ Capable of secreting antigen binding immunoglobulin Millions of genetically different clones of B cell responding to different antigens Recognising right antigen -proliferation of clone, differentiation to plasma cell, generation of memory cells |
| T helper cells | CD3+ CD4+ CD8- recognise professional antigen presenting cells Specificity - MHC Class II - peptide combination Secrete cytokines that promote or modulate the responses of other cells e.g. IL2 |
| Cytotoxic T cells | CD3+ CD4- CD8+ Recognise virus infected cells Specificity - MHC class I peptide complex Secrete toxic granules to site of recognition Kill infected cells |
| Leukocyte antigen interactions | CD4+ helper cell activates B cells It also activates cytotoxic T cells and mature DCs It is stimulated itself by mature DCs This is done by the secretion of cytokines specific for each cell type |
| Deficiency of T lymphocytes | DiGeorge syndrome Deletion of 22q 11.2 leads to loss of thymus development No adaptive immunity - except some thymus independent antibodies No graft rejection |
| Deficiency of B lymphocytes | X linked agammaglobulinemia Mutation in Bruton Tyrosine kinase No antibodies - numerous infections |
| Deficiency of all lymphocytes | Severe combined immunodeficiency Many variants e.g. ADA-SCID lack of adenosine deaminase No adaptive immunity No graft rejection |
| Deficiency of all phagocytes | Chronic granulomatous disease X linked and autosomal recessive - deficiency in phagolysosome killing component Phagocytes fail to kill bacteria - recurrent pyogenic infection |
| Deficiency of neutrophils | Chediak-Higashi syndrome Autosomal recessive - failure to mature granulocytes Neutropenia - recurrent pyogenic infections |
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