Question

During these disorders, neutrophils (a type of leukocyte) adhered to the vascular endothelium and then migrated into surrounding tissues. The adherence of neutrophils was facilitated by an adhesion receptor on the neutrophil membrane

A neutrophil has point mutations in the genes coding for the alpha and the beta subunits of the adhesion receptor. However, this cell can still migrate through endothelium. Which of the following conclusions about the effect of this mutation can be drawn?
A. The cell cannot release toxic products such as prostaglandins.
B. The cell has only functional beta subunits.
C. The cell can bind to endothelium.
D. The cell has a defective cell membrane.

Answer 1

The most accurate conclusion from the given scenario is that the neutrophil can still bind to endothelium despite having mutations in the adhesion receptor genes. This indicates that the neutrophil retains the ability to migrate through the endothelium, likely using other compensatory mechanisms or partial functionality of the mutated receptors.

Step-by-step explanation:

The question concerns the ability of neutrophils to migrate through endothelium despite point mutations in the genes coding for the alpha and beta subunits of the adhesion receptor. If neutrophils with these mutations can still migrate, it suggests that the mutated receptors may retain some functionality or that there may be other mechanisms at play that facilitate the migration. The most accurate conclusion that can be drawn from the information provided is that:

• The cell can bind to endothelium (Option C).

This conclusion is supported by the fact that the neutrophil can still migrate through the endothelium. Functions such as releasing toxic products like prostaglandins, having only functional beta subunits, and having a defective cell membrane do not directly pertain to the ability to migrate, which is the focus of the question. It should be noted that leukotrienes play a significant role in attracting neutrophils to the site of infection, suggesting other pathways could compensate for dysfunctional adhesion receptors.