TL;DR: The proper formation of granulomas to wall off TB requires CD4 Th1 cells and marcophages

TB (mycobacterium tuberculosis) begins its life cycle inside of the lungs by being phagocytized by alveolar macrophages abd undergoing intracellular growth and replication within the macrophages. NONactivated macrophages lack the ability to kill TB. In a normal person, some of the macrophages will present TB antigens to CD4 cells and secrete IL12, inducing differentiation to Th1 cells which will then begin the process of granuloma formation. No CD4 T-lymphocytes means no activation of macrophages for granuloma formation, so the macrophages will have deficient function.

FA2020 p217 has the steps of granuloma formation:

• APCs present antigens to CD4 helper T-cells and secrete IL12 to cause differentiation into Th1 cells
• Th1 cells secrete IFNgamma to activate macrophages and induce granuloma formation
• Activated macrophages have better intracellular killing of pathogens such as TB and will increase cytokine secretion (e.g. TNFalpha) to cause formation of epitheliod macrophages and giant cells
• TNFalpha is necessary for maintenance of granulomas

NOTE: Langhans giant cells are formed by activated macrophages after granuloma formation has been already been initiated

Also noteworthy:

Macrophages are attracted to the area of PPD exposure via the action of Th1 lymphocytes in patients previously exposed to MTB. They are the predominant cell type found at the site of PPD exposure (the area of skin injection at 48 hours, when it's read) and also in the lungs of patients with pulmonary tuberculosis.