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Endocrinology > Exam 4 Lecture 26 Immune/endo/CNS > Flashcards

Exam 4 Lecture 26 Immune/endo/CNS Flashcards

1
Q

Leukocytes and Neutrophils

A

Produced in bone marrow.
Functions:
1. phagocytosis
2. Release chemicals involved in inflammation (vasodilator, chemotaxins, etc.)

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2
Q

Basophils

A

Produced in bone marrow

Have functions in blood similar to those of mast cells in tissues

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3
Q

Eosinophils

A

Produced in bone marrow
Functions:
1. Destroy multicellular parasites
2. Participate in immediate hypersensitivity reactions

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4
Q

Monocytes

A

Produced in bone marrow
Functions
1. Have functions in blood similar to those of macrophages in tissues
2. Enter tissues and are transformed into macrophages

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5
Q

Lymphocytes

A

Mature in bone marrow (B cells and NK cells) and thymus (T cells); activated in peripheral lymphoid organs
Function:
serve as “recognition cells” in specific immune responses and are essential for all aspects of these responses

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6
Q

B cells

A

Mature in bone marrow; activated in peripheral lymphoid organs
Functions:
1. initiate antibody-mediated immune responses by binding specific antigens to the B cell’s plasma membrane receptors, which are immunoglobulin
2. During activation are transformed into plasma cells, which secrete antibodies
3. Present antigen to helper T cells

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7
Q

Cytotoxic T cells (CD8 cells)

A

Mature in thymus
Functions:
bind to antigens on plasma membrane of target cells (virus-infected cells, cancer cells, and tissue transplants) and directly destroy the cells

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8
Q

Helper T cells (CD4 cells)

A

Mature in thymus

Functions: Secrete cytokines that help to activate B cells, Cytotoxic T cells, NK cells and macrophages

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9
Q

NK cells

A

Mature in bone marrow
Functions:
1. Bind directly and nonspecifically to virus-infected cells and cancer cells and kill them
2. function as killer cells in antibody-dependent cellular cytotoxicity (ADCC)

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10
Q

Plasma cells

A

Produced in peripheral lymphoid organs; differentiate from B cells during immune responses
Secrete antibodies

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11
Q

Macrophages

A

Produced in bone marrow, reside in almost all tissues and organs; differentiate from monotypes
Functions:
1. Phagocytosis
2. Extracellular killing via secretion of toxic chemicals
3. Process and present antigens to helper T cells
4. Secrete cytokines involved in inflammation, activation and differentiation of helper T cells, and systemic responses to infection or injury (the acute phase response)

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12
Q

Macrophage-like cells

A

Almost all tissues and organs; microglia in the CNS

Functions: same as macrophages

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13
Q

Mast cells

A

Produced in bone marrow; reside in almost all tissues and organs; differentiate from bone marrow cells
Functions: release histamine and other chemicals involved in inflammation

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14
Q

What stimuli does immune system respond to?

A

Bacteria, viruses, tumors and other antigens

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15
Q

What happens when immune system is stimulated?

A

Cell- mediated or numeral immune responses are activated and this information is sent to the hypothalamus by cytokines and peptide hormones secreted from cells of the immune system

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16
Q

How might immune system signaling and activation be communicated to the nervous system?

A

Through the release of peripheral soluble factors (particularly cytokines) by cells of the immune system. These factors function as hormones to affect the CNS.

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17
Q

How can peripheral soluble factors affect the CNS?

A

Directly by crossing the BBB or indirectly by stimulation of the vagus nerve

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18
Q

Two types of signaling molecules between immune and CND or PNS?

A

Cytokines or chemokines

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19
Q

How can cytokines directly influence the electrophysiological function of neurons in the CNS or PNS?

A

During inflammation of the brain or PNS

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20
Q

What is the family of chemokines associated with?

A

The trafficking of leukocytes in physiological immune surveillance and inflammatory cell recruitment in host defense.

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21
Q

How are chemokines expressed in CNS?

A

constitutively by microglia cells, osteocytes and neurons and their expression can be increased after induction with inflammatory mediators.

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22
Q

What in CNS can chemokines modulate?

A

Neuronal signaling through the inhibition of neuronal calcium currents

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23
Q

Four cytokine categories

A
  1. Inflammatory cytokines
  2. immunomodulatory cytokines
  3. chemokines
  4. Growth factors and other mediators`
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24
Q

What can cytokines released by immune system influence in CNS?

A

Cognitive processes, central neurotransmission and the function of the PNS

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25
Q

Which cytokines and neuropeptides have effects on behavior that is mediated by the CNS?

A

Those secreted by peripheral immune cells

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26
Q

How can pro=inflammatory cytokines activate the hypothalamus-pituitary-adrenal axis and induce sickness behavior during the acute phase response?

A

Fever, sickness behavior, depressive effects on social behavior

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27
Q

What organs are affected by systemic response to infection or injury?

A

Brain, Liver, Bone marrow, Adipose tissue, muscle, hypothalamus, anterior pituitary, adrenal cortex

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28
Q

What happens immediately after microbe infection or injury?

A

Monotypes and macrophages secret IL-1, TNS and IL 6, which increases Plasma IL-1, TNS and IL-6

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29
Q

How do IL-1, TNF and IL-6 affect the brain?

A

Fever, decreased appetite and food intake, sleepiness, fatigue

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30
Q

How do IL-1, TNS and IL-6 affect the liver?

A

Liver retains Fe, Zn, secretes acute phase proteins. All these things change in plasma.

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31
Q

How do IL-1, TNS and IL-6 affect bone marrow?

A

Cause production and release of leukocytes and increase in blood leukocytes

32
Q

How do IL-1, TNS and IL-6 affect adipose tissue?

A

Increase lipolysis and increase plasma free fatty acids

33
Q

How do IL-1, TNS and IL-6 affect muscle?

A

Increase in protein breakdown and aa release. Increase in plasma amino acids.

34
Q

How do IL-1, TNS and IL-6 affect hypothalamus and anterior pituitary? Adrenal cortex?

A

ACTH secretion increases as well as plasma ACTH. Adrenal cortex increases cortisol secretion. Plasma cortisol increases.

35
Q

How do cytokines work on endocrine glands?

A

Cytokines act directly on endocrine glands such as the pituitary, thyroid, pancreas, Adrenals and gonads and alter their secretions.

36
Q

How do pituitary hormones influence immune function?

A

Pituitary hormones and secretions of their peripheral target endocrine glands may modulate immune function.

37
Q

How ACTH/glucocorticoids related to immune system?

A

They are immunosuppressants

38
Q

How do GH and prolactin influence immune system?

A

Gh and Prolactin may potentate immune responses through a variety of effects and can stimulate growth and activity of the thymus gland.

39
Q

What do cognitive stimuli like stress stimulate?

A

neuroendocrine pathways GH, PRL, and adrenal, Gonadal and thyroid hormones, trophic hormones

40
Q

What effect do adrenal, Gonadal and thyroid hormones and trophic hormones have on B and T cells?

A

They can up or downregulate them.

41
Q

What effect can GH and PRL have on T cells?

A

Unregulate them.

42
Q

What can T cells stimulate?

A

cytokines

43
Q

What effect do adrenal, Gonadal and thyroid hormones, trophic hormones have on thymus?

A

Unregulated the secretion of thymic hormones.

44
Q

What do thymic hormones stimulate?

A

T cells and cytokines

45
Q

How do thymic hormones affect brain?

A

Provide feedback

46
Q

How do T cells affect brain?

A

Provide feedback via proteins ad peptide hormones secreted by immune cells

47
Q

What do non-cognitive stimuli, like antigens, stimulate?

A

The release of macrophages, which stimulate cytokines

48
Q

How do we know that the hypothalamic-pituitary-adrenal axis affects the immune system?

A

Surgical removal of pituitary lad to reduced antibody responses. GH treatment restored antibody production.

49
Q

How does ACTH influence immune system?

A

There are ACTH receptors on both B. ad T cells. ACTH also reduces antibody responses in vitro and reduced IFN-gamma (interferon) production

50
Q

What stimulates prolactin synthesis in hypothalamus?

A

Suckling stimulus, sleep, stress

51
Q

How does TRH or (VIP) from hypothalamus influence release of prolactin?

A

Unregulated it

52
Q

How does dopamine or somatostatin influence prolactin release?

A

downregulates it

53
Q

How do estrogens influence pituitary prolactin release?

A

It unregulated it

54
Q

What kind of feedback does pituitary provide hypothalamus regarding prolactin?

A

Negative feedbac

55
Q

How does prolactin affect immune system?

A

Lymphocytes: regulation, e.g. Nb2 cells

56
Q

Hypothalamus-pituitary-adrenal axis

A
  1. hypothalamic releasing factors: CRH and vasopressin
  2. Pituitary secretes corticotropin (ACTH) to stimulate adrenal cortex
  3. Adrenal gland releases steroid hormones
  4. Feedback inhibition by cortisol of monocyte and TNFalpha, IL-6, IL-2, IL-1 release and of macrophages and IL-1-RA release
57
Q

Following injury or response to infection, what do cells in local tissues release?

A

Cytokines that travel via the bloodstream to the liver and the CNS

58
Q

How else might information about injury be sent to CNS?

A

Via affront neural pathways, including the vague nerve and nociceptive fibers

59
Q

What does activation of the HPA by IL-6 (cytokine) do?

A

Increase the secretion of adrenocorticotropin (ACTH), which in turn increases cortisol release from the adrenal cortex.

60
Q

What does increased activity along sympathetic nerves do?

A

It enhances the release of epinephrine from the adrenal medulla

61
Q

What kind of immune activity do cortisol and EPI perform in bloodstream?

A

anti-inflammatory

62
Q

Of what do IL-6 and other cytokines stimulate the production of?

A

Acute phase proteins. They also activate the other features of the acute phase response.

63
Q

What does efferent activity along the vague nerve release?

A

Acetylcholine, which inhibits the production of tumor necrosis factor (TNF) and other pro-inflammatory molecules by Kupffer cells and other tissue-resident macrophages

64
Q

How do cytokines activate pituitary croticotrophs?

A

In a corticotroph, specific binding of selected cytokines to gp130-linked transmembrane spanning receptors mediates activation of JAK-STAT pathway, increased POMC gene transcription, and increased ACTH secretion.

65
Q

What does increasing circulation of EPI do response to an endotoxin by immune system?

A

It converts an inflammatory (TNF dominant) response to anti-inflammatory (IL-10 dominant).

66
Q

What anti-inflammatory properties does ACTH have?

A

ACTH, cortisol and the synthetic analogs of cortisol have the capacity to prevent or suppress the development of local heat, redness, swelling, and tenderness by which inflammation is recognized at the gross level of observation.

67
Q

How do ACTH and its analogs prevent inflammation?

A

At the microscopic level, they inhibit early phenomena of inflammatory process (edema, fibrin deposition, capillary dilatation, migration of leukocytes into the inflamed area, and phagocytic activity). Also later manifestations (capillary proliferation, fibroblast proliferation, deposition of collagen, and still later, cicatrization)

68
Q

Inflammation axis

A
  1. Stimulus: bacteria, virus, fungus, trauma, immune challenge
  2. Primary inflammatory: cytokines (IL-1beta, TNF-alpha)
  3. inflammation
69
Q

What is produced during inflammatory response?

A
  1. IL-1beta, TNF-alpha, More cytokines
  2. eicosanoids (prostaglandins leukotrienes)
  3. platelet activating factor
  4. Neuropeptides
  5. Various other mediators
70
Q

How do inflammatory agents influence HAP?

A

Hypo releases CRH and LHRH
Pituitary releases ACTH, gonadotropin, TSH, prolactin, growth hormone
Adrenal releases cortisol and catecholamines

71
Q

How do inflammatory agents influence liver?

A

Produces acute phase proteins

72
Q

How do Gonadal steroids influence immune system and regulation of neuronal gene expressions?

A

Androgens generally exert suppressive effects on both humoral and cellular immune response and seem to represent natural anti-inflammatory hormones.
Estrogens, on the other hand, exert immunoenhancing activities, at least on humoral immune response

73
Q

What kind of sexual dimorphism exists within the immune system?

A

Females have higher levels of IgG, IgM and IgA than males.

74
Q

In what gender is antibody response to antigen greater in magnitude?

A

Females. More prolonged, too.

75
Q

How much more autoimmune disease do females experience?

A

Two to tenfold higher incidence

76
Q

How do testosterone and estrogen alter disease progression?

A

Manipulation of testosterone or estrogen alters autoimmune disease progression or onset in animal models.

Endocrinology (21 decks)

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