X-Linked Severe Combined Immunodeficiency (SCID) stems from a mutation in either common γ chain gene or IL-7 receptor-α gene. A mutation in the common γ chain gene leads to an inability to bind (and hence respond) to cytokines IL-2,4,7,9,15,21. Without activity of those cytokines, the individual cannot produce T cells, B cells nor NK cells; the patient has bubble boy disease and almost no ability to fend off infection. A mutation in the IL-7 receptor-α gene leads to a lack of T cells but present B cells and NK cells. Based on this -- and the paragraph above -- it is clear that IL-7 is critical for T cell formation, but not B cell nor NK cell formation.
It is worth noting that mice require IL-7 for both T cell and B cell formation. SCID mice are extremely useful research tools. Lacking B and T cells, they are unable to mount an adaptive immune response. Thus, they do not reject transplanted tissues and are also useful for studying how to restore hematopoiesis. Also, SCID has been successfully treated via gene therapy techniques to introduce a functioning common γ chain gene into hematopoietic stem cells.