class 2 2

Question 1

Describe the role of chemokines in orchestrating the migration of leukocytes.

Answer 1

Chemokines govern the directed migration of leukocytes during homeostasis, tumour development, and inflammation, orchestrating their migratory activities.

Question 2

What are some ways to enhance or reduce leukocyte migration mediated by chemokines?

Answer 2

Leukocyte migration mediated by chemokines can be enhanced or reduced through posttranslational modifications.

Question 3

Define chemokine synergy and its impact on leukocyte influx during an inflammatory response.

Answer 3

Chemokine synergy is a positive regulatory mechanism that rapidly augments the local leukocyte influx, thereby enhancing the outcome of an inflammatory response in vivo.

Question 4

How are chemokine and/or receptor heterodimerization involved in the cellular mechanisms of chemokine synergy?

Answer 4

Chemokine and/or receptor heterodimerization are debated cellular mechanisms involved in chemokine synergy, potentially leading to cooperation in signal transduction.

Question 5

Describe the essential triggers for the regulation of cytokine and chemokine production.

Answer 5

The regulation of cytokine and chemokine production is triggered by inflammatory or infectious stimuli recognized by pattern recognition receptors (PRRs), Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-like receptors (RLRs).

Question 6

Describe the synergy chemokines in leukocyte adhesion and migration.

Answer 6

Chemok can work together to the local leukocyte influx, thereby improving the outcome of an inflammatory response.

Question 7

What are some proposed mechanisms for the synergy between chemokines in leukocyte migration?

Answer 7

Proposed mechanisms include chemotaxis, adhesion, intracellular calcium rise, ERK phosphorylation, and receptor internalization.

Question 8

Define chemokine synergy.

Answer 8

Chemokine synergy refers to the cooperative interaction between different chemokines to enhance leukocyte responses such as migration and adhesion.

Question 9

How do chemokines interact with glycosaminoglycans (GAG) on endothelial cells?

Answer 9

Chemokines can form dimers after binding to GAG on endothelial cells.

Question 10

What are some examples of dual receptor-mediated chemokine synergy?

Answer 10

Examples involve two types of chemokine receptors simultaneously or sequentially exposed to their agonists.

Question 11

Describe the synergistic effect between CCL5 and CXCL12 on monocytes.

Answer 11

The synergistic effect between CCL5 and CXCL12 on monocytes involves the inhibition of leukocyte migration and is evidence for a dual receptor-related synergism.

Question 12

Define chemokine heterodimerization and its relation to the enhancement of leukocyte migration.

Answer 12

Chemokine heterodimerization refers to the formation of heteromers by two different chemokines, which can significantly alter their biological activities and enhance leukocyte migration.

Question 13

How does heterodimerization of CXCL8 and CXCL4 affect the chemotactic capacity of CXCL8 on the Baf3 cell line?

Answer 13

Heterodimerization of CXCL8 and CXCL4 increases the chemotactic capacity of CXCL8 on the Baf3 cell line, which consists of bone marrow-derived pro-B-cells transfected with CXCR1 and CXCR2.

Question 14

Do chemokines co-expressed with CCL22 at specific sites in the inflamed skin exert synergism via CCR4 activation?

Answer 14

Yes, chemokines co-expressed with CCL22 at specific sites in the inflamed skin can synergize via CCR4 activation, as observed in the migration of CCR4+ lymphocytes.

Question 15

Describe the role of CCL19 and CCL21 in enhancing CCL7-induced migration on monocytes.

Answer 15

CCL19 and CCL21, known as homeostatic chemokines, enhance CCL7-induced migration on monocytes, as demonstrated by Kuscher et al.

Question 16

What is the potential responsibility of coexpression and heterocomplex formation between CXCL9 and CXCL12 in the tumour vasculature of primary central nervous system lymphomas (PCNSL)?

Answer 16

The coexpression and heterocomplex formation between CXCL9 and CXCL12 in the tumour vasculature of PCNSL might be responsible for a synergistic increase in leukocyte migration, as demonstrated by Venetz et al.

Question 17

Describe the process of chemokine heterodimer formation and its impact on function at the quaternary structural level.

Answer 17

Chemokine heterodimer formation involves the association of CXC and CC chemokines, which modulates function at the quaternary structural level.

Question 18

What are the therapeutic implications of targeting chemokine interactions in atherosclerosis?

Answer 18

Therapeutic targeting of chemokine interactions in atherosclerosis has potential implications for treatment and management of the condition.

Question 19

How does a rich chemokine environment enhance leukocyte migration and activities?

Answer 19

A rich chemokine environment strongly enhances leukocyte migration and activities.

Question 20

Define synergy-inducing chemokines and explain how they enhance CCR2 ligand activities on monocytes.

Answer 20

Synergy-inducing chemokines enhance CCR2 ligand activities on monocytes, potentially impacting monocyte function.

Question 21

Describe the distinct signaling pathways activated by chemokine receptor homo- or hetero-dimerization.

Answer 21

Chemokine receptor homo- or hetero-dimerization activates distinct signaling pathways.

Question 22

What evidence exists for negative binding cooperativity within CCR5-CCR2b heterodimers?

Answer 22

Evidence exists for negative binding cooperativity within CCR5-CCR2b heterodimers.

Question 23

How do CXCR4-CCR5 heterodimers modulate T cell functions?

Answer 23

CXCR4-CCR5 heterodimers function as a couple modulating T cell functions.

Question 24

What does fluorescence resonance energy transfer imaging reveal about chemokine-binding and its impact on CXCR4 and CCR5 receptor heterodimers?

Answer 24

Fluorescence resonance energy transfer imaging reveals that chemokine-binding modulates heterodimers of CXCR4 and CCR5 receptors.