Provided herein is a method of treating bone resorption associated with osteoclastic activity in a subject in need thereof. The method includes reducing the level of FMS intracellular fragments (FICDs) in the subject.

The present disclosure relates generally to compositions and methods for diagnosing and treating idiopathic pulmonary fibrosis (IPF). Also, methods for identifying IPF disease severity and likelihood for disease progression. An IPF patient can be identified when the CSF1 concentration or soluble CSF1R concentration in a blood sample is decreased as compared to a reference blood sample from a reference human subject not having IPF, and/or when the soluble CSF1R concentration in a bronchoalveolar lavage (BAL) fluid sample is increased as compared to a reference BAL fluid sample from the reference human subject. Once identified, the patient can be treated with, for instance, CSF1 or CSF1R inhibitors, such as antibodies. Moreover, the IPF patient soluble CSF1R level in blood or BAL samples can also be used to assess the severity of disease, and to both monitor disease progression and treatment outcomes.

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is caused by dominant inactivating mutations in the colony stimulating factor receptor 1 (CSF1R) kinase domain. GM-CSF haploinsufficiency corrects olfactory, cognitive and emotional functions lost in Csf1r+/− mice. This correlates with the correction of microgliosis and microglial functions resulting in improvement of myelination and rescue of neurogenesis. However, GM-CSF haploinsufficiency fails to correct the motor deficits of Csf1r+/− mice and cerebellar microgliosis. The present invention discloses methods and compositions using GM-CSF as a suitable therapeutic target to inhibit in amelioration of the cognitive impairments in ALSP and other in conditions involving inflammatory activation of microglia and macrophages, such as AD, ALS, multiple sclerosis, and hippocampal inflammation following radiation therapy. Treatment with GM-CSF inhibitors is beneficial in ALSP, as adult neurogenesis is important for memory, olfaction and prevention of anxiety/depression and early initiation of such treatment in carriers of CSF1R mutations may increase effectiveness. Balancing the actions of CSF-1R and GM-CSF signaling are necessary to preserve olfaction, cognition and emotional balance in aged mice. This balance is likely altered in many neurodegenerative diseases in which activated microglia contribute to the pathology.

The present invention relates to a method for the diagnosis of sarcoidosis. In particular, the present invention relates to a method for the differential diagnosis of sarcoidosis versus tuberculosis infection.

Described are methods and compositions for evaluating the relapse risk n subjects having an inflammatory bowel disease (IBD). Some embodiments include selecting a treatment for an evaluated IBD relapse risk in a subject.

Described herein are methods of treating cancers and other tumors related to the decreased proliferation, the depletion, or the repolarization of tumor-associated macrophages (TAMs) and treatment of associated disorders, including tenosynovial giant cell tumor (TGCT) and diffuse-type tenosynovial giant cell tumor (DTGCT).