Inflammation activates the complement pathway that will clear the infection

Inflammation increases the local accumulation of neutrophils, and reduces the amount of fluid, at the site of infection

Inflammation increases the local accumulation of dendritic cells to collect antigen, and that can then leave the infected area due to chemokines

Inflammation increases the accumulation of leukocytes, fluid, and plasma proteins at the site of infection

1: Basophil, 2: Lymphocyte, 3: Basophil, 4: Neutrophil

1: Neutrophil, 2: Macrophage, 3: Lymphocyte, 4: Basophil

1: Neutrophil, 2: Lymphocyte, 3: Eosinophil, 4: Basophil

1: Eosinophil, 2: Lymphocyte, 3: Neutrophil, 4: Basophil

The range of unique antigen receptors associated with lymphocytes

The range of different effector mechanisms that the immune system employs

The range of anatomical locations that the immune system is able to access

The range of different immune cells in the immune system

 By active transport through endoplasmic pores

 Via the proteasome-induced ER pore

 Via the transporter associated with antigen-processing

 Via the ER translocase

B cell

NK cell

Macrophage

T cell

1: Eosinophil, 2: Lymphocyte, 3: Neutrophil, 4: Basophil

1: Lymphocyte, 2: Basophil, 3: Neutrophil, 4: Eosinophil

1: Basophil, 2: Lymphocyte, 3: Eosinophil, 4: Neutrophil

1: Neutrophil, 2: Lymphocyte, 3: Eosinophil, 4: Basophil

In order to be functional, caspace-1 must first be cleaved to a smaller molecule.

Pro-IL-1b is active but must be cleaved to be secreted from the cell.

The inflammasome is only activated upon contact or detection of microbial products.

Within the cell, different triggers of the inflammasome will lead to the production of different inflammatory cytokines.

The CD8 molecule binds to the MHC I molecule.

The CD4 molecule does not bind to the MHC class

I molecule

The TCR binds to the MHC class I molecule

This is a false statement because TCR will not

bind to MHC presenting self-peptides