People affected by GLILD may have symptoms such as cough and breathlessness, but may also be asymptomatic, with the condition first detected through abnormalities on lung function tests or a CT scan of the lungs.

Granulomatous–lymphocytic interstitial lung disease (GLILD) is a lung complication of common variable immunodeficiency disorders (CVID). It is seen in approximately 15% of patients with CVID. It has been defined histologically as the presence of (non-caseating) granuloma and lymphoproliferation in the lung. However, as GLILD is often associated with other auto-immune features such as splenomegaly, adenopathy and cytopenias, a definition based on abnormalities on lung imaging (CT scan) together with evidence of granulomatous inflammation elsewhere has also been employed.

Although infections and complications of infection such as bronchiectasis are more common complications of CVID in the lung, the presence of immune manifestations including GLILD is important because this has been associated with greater risk of death.

In general, as a rare complication of a rare disease, the condition remains incompletely understood, and there is real need for further research in the area.

Most common:

- Chest Pain

- Cough

- Fever

- Shortness of breath

- Joint pain, stiffness, swelling

- Skin nodules

People may not present with all these symptoms or non at all.

The typical symptoms of UIP are progressive shortness of breath and cough for a period of months. In some patients, UIP is diagnosed only when a more acute disease supervenes and brings the patient to medical attention.

In patients with lymphocytic interstitial pneumonia, these patients may present with lymphadenopathy, enlarged liver, enlarged spleen, enlarged salivary gland, thickening and widening of the extremities of the fingers and toes (clubbing), and breathing symptoms such as shortness of breath and wheezing.

Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered on the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.

When the nodules are centered on the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.

These findings appear soon after the onset of symptoms and change rapidly thereafter.

A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.

The signs and symptoms of PAP include shortness of breath, a cough, low grade fever, and weight loss.

The clinical course of PAP is unpredictable. Spontaneous remission is recognized, and some patients have stable symptoms. Death may occur due to the progression of PAP or of any underlying associated disease. Individuals with PAP are more vulnerable to lung infections such as bacterial pneumonia, mycobacterium avium-intracellulare infection, or a fungal infection.

The cause of the scarring in UIP may be known (less commonly) or unknown (more commonly). Since the medical term for conditions of unknown cause is "idiopathic", the clinical term for UIP of unknown cause is idiopathic pulmonary fibrosis (IPF). Examples of known causes of UIP include systemic sclerosis/scleroderma, rheumatoid arthritis, asbestosis, and prolonged use of medications such as nitrofurantoin or amiodarone.

Alveolar lung disease may be divided into acute or chronic. Causes of acute alveolar lung disease include pulmonary edema (cardiogenic or neurogenic), pneumonia (bacterial or viral), pulmonary embolism, systemic lupus erythematosus, bleeding in the lungs (e.g., Goodpasture syndrome), idiopathic pulmonary hemosiderosis, and granulomatosis with polyangiitis.

Chronic alveolar lung disease can be caused by pulmonary alveolar proteinosis, alveolar cell carcinoma, mineral oil pneumonia, sarcoidosis (alveolar form), lymphoma, tuberculosis, metastases, or desquamative interstitial pneumonia.

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

Pulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis, respiratory broncholitis associated with interstitial lung disease.

- Lower lung predominance

Idiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

- Central predominance (perihilar)

Sarcoidosis, berylliosis

- Peripheral predominance

Idiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

Classification can be complex, and the combined efforts of clinicians, radiologists, and pathologists can help in the generation of a more specific diagnosis.

Idiopathic interstitial pneumonia can be subclassified based on histologic appearance into the following patterns:

Usual interstitial pneumonia is the most common type.

Rheumatoid Lung Disease, also called Rheumatoid Lung is a disease of the lung associated with RA, rheumatoid arthritis. Rheumatoid lung disease is characterized by pleural effusion, pulmonary fibrosis, lung nodules and pulmonary hypertension. Common symptoms associated with the disease include shortness of breath, cough, chest pain and fever. It is estimated that about one quarter of people with rheumatoid arthritis develop this disease, which are more likely to develop among elderly men with a history of smoking.

Rheumatoid lung is separate from but often associated with Interstitial lung disease(ILD).

Lymphocytic interstitial pneumonia (also called lymphocytic interstitial pneumonitis or LIP) is a syndrome secondary to autoimmune and other lymphoproliferative disorders. Symptoms include fever, cough, and shortness of breath. Lymphocytic interstitial pneumonia applies to disorders associated with both monoclonal or polyclonal gammopathy.

Pulmonary alveolar proteinosis (PAP) is a rare lung disease in which an abnormal accumulation of pulmonary surfactant occurs within the alveoli (microscopic air sacs in the lung), interfering with the lungs' ability to exchange oxygen from the air, and carbon dioxide from the blood. PAP can occur in a primary form or secondarily in the settings of certain cancers (such as myeloid leukemia), lung infections, or environmental exposure to dusts or chemicals. Rare familial forms have also been recognized, suggesting a genetic component in those cases.

The most common symptoms of acute interstitial pneumonitis are highly productive cough with expectoration of thick mucus, fever, and difficulties breathing. These often occur over a period of one to two weeks before medical attention is sought. The presence of fluid means the person experiences a feeling similar to 'drowning'. Difficulties breathing can quickly progress to an inability to breathe without support (respiratory failure).

Acute interstitial pneumonitis typically progresses rapidly, with hospitalization and mechanical ventilation often required only days to weeks after initial symptoms of cough, fever, and difficulties breathing develop.

Idiopathic interstitial pneumonia (IIP), or noninfectious pneumonia are a class of diffuse lung diseases. These diseases typically affect the pulmonary interstitium, although some also have a component affecting the airways (for instance, Cryptogenic organizing pneumonitis). There are seven recognized distinct subtypes of IIP.

In many patients, symptoms are present for a considerable time before diagnosis. The most common clinical features of IPF include the following:

- Age over 50 years

- Dry, non-productive cough on exertion

- Progressive exertional dyspnea (shortness of breath with exercise)

- Dry, inspiratory bibasilar "velcro-like" crackles on auscultation (a crackling sound in the lungs during inhalation similar to Velcro being torn apart slowly, heard with a stethoscope).

- Clubbing of the digits, a disfigurement of the finger tips or toes (see image)

- Abnormal pulmonary function test results, with evidence of restriction and impaired gas exchange.

Some of these features are due to chronic hypoxemia (oxygen deficiency in the blood), are not specific for IPF, and can occur in other pulmonary disorders. IPF should be considered in all patients with unexplained chronic exertional dyspnea who present with cough, inspiratory bibasilar crackles, or finger clubbing.

Assessment of "velcro" crackles on lung auscultation is a practical way to improve the earlier diagnosis of IPF. Fine crackles are easily recognized by clinicians and are characteristic of IPF.

If bilateral fine crackles are present throughout the inspiratory time and are persisting after several deep breaths, and if remaining present on several occasions several weeks apart in a subject aged ≥60 years, this should raise the suspicion of IPF and lead to consideration of an HRCT scan of the chest which is more sensitive than a chest X-ray. As crackles are not specific for IPF, they must prompt a thorough diagnostic process.

Non-specific interstitial pneumonia (NSIP) is a form of idiopathic interstitial pneumonia.

The fibrosing pattern of NSIP has a five year survival rate of 86% to 92%, while the cellular pattern of NSIP has a 100% five year survival rate. Patients with NSIP(whether cellular or fibrosing), have a better prognosis than those with usual interstitial pneumonia (UIP).

Acute interstitial pneumonitis (also known as acute interstitial pneumonia or Hamman–Rich syndrome) is a rare, severe lung disease that usually affects otherwise healthy individuals. There is no known cause or cure.

Acute interstitial pneumonitis is often categorized as both an interstitial lung disease and a form of acute respiratory distress syndrome (ARDS) but it is distinguished from the "chronic" forms of interstitial pneumonia such as idiopathic pulmonary fibrosis.

Symptoms of pulmonary fibrosis are mainly:

- Shortness of breath, particularly with exertion

- Chronic dry, hacking coughing

- Fatigue and weakness

- Chest discomfort including chest pain

- Loss of appetite and rapid weight loss

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high-resolution CT will frequently demonstrate abnormalities.

Idiopathic pulmonary fibrosis (IPF) is a chronic irreversible and ultimately fatal disease characterized by a progressive decline in lung function. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This official statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was approved by the ATS board of directors, June 2013 and by the ERS Steering Committee, March 2013. "Am Respir Crit Care Med." 188 (6): 733–748. September 15, 2013. The term pulmonary fibrosis means scarring of lung tissue and is the cause of worsening dyspnea (shortness of breath). Fibrosis is usually associated with a poor prognosis.

IPF belongs to a large group of more than 200 lung diseases known as interstitial lung diseases (ILDs), characterized by the involvement of lung interstitium. The interstitium, the tissue between the air sacs in the lung, is the primary site of injury in ILDs. However, these disorders frequently affect not only the interstitium, but also the airspaces, peripheral airways, and vessels. Lung tissue from people with IPF shows a characteristic histopathologic pattern known as usual interstitial pneumonia (UIP). UIP is therefore the pathologic counterpart of IPF. The term 'idiopathic' is used because the cause of pulmonary fibrosis is still unknown. IPF usually occurs in adults of between 50 and 70 years of age, particularly those with a history of cigarette smoking, and affects more men than women. The diagnosis of IPF requires exclusion of other known causes of ILDs and the presence of a typical radiological pattern identified through high resolution computed tomography (HRCT). In the right clinical setting, it is possible to make the diagnosis of IPF by HRCT alone, obviating the need for surgical lung biopsy.

Treatment to slow down the progression of the disease may include nintedanib or pirfenidone.

The major signs of indium lung are pulmonary alveolar proteinosis and pulmonary fibrosis. Symptoms include dyspnea (shortness of breath), cough, and increased sputum production. Hemoptysis has also been seen in people with indium lung. Other symptoms seen in some but not all cases include digital clubbing, low DLCO (capacity to move oxygen from the alveoli into the blood), and lowered forced expiratory volume. Emphysema has been associated with indium lung, but may not be part of the syndrome.

Signs and symptoms of flock worker's lung include rales (crackling noises caused by fluid in the lungs), dyspnea (shortness of breath), and coughing. Abnormalities seen on a computed tomography (CT) scan of the lungs can include ground glass opacity and reticular opacity. The typical histopathology in flock worker's lung is bronchiolocentric interstitial pneumonitis and lymphocytic bronchiolitis with lymphocytic hyperplasia. Occasionally, desquamative interstitial pneumonia and bronchiolitis obliterans organizing pneumonia can be seen.

Other symptoms described in flock workers include pleuritic chest pain and atypical chest pain. Most cases described have been chronic and progressive. Lung function in individuals with flock worker's lung is generally diminished, with both restrictive and obstructive defects found.